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Juei-tang Cheng - One of the best experts on this subject based on the ideXlab platform.

  • Improvement of Insulin resistance by miracle fruit (Synsepalum dulcificum) in fructose-rich chow-fed rats.
    Phytotherapy Research, 2020
    Co-Authors: Chang-chih Chen, Juei-tang Cheng
    Abstract:

    In an attempt to probe a new target to improve Insulin resistance, miracle fruit (Synsepalum dulcificum) was employed to investigate the effect on Insulin resistance induced by fructose-rich chow in rats. Single oral administration of the powder of this miracle fruit decreased the plasma glucose in a dose-dependent manner for 150 min in rats fed fructose-rich chow for 4 weeks. Insulin action on the glucose disposal rate was measured using the glucose-Insulin Index, the value of the areas under the curve of glucose and Insulin during the intraperitoneal glucose tolerance test. Oral administration of miracle fruit (0.2 mg/kg) to fructose-rich chow fed rats, three times daily for 3 days, reversed the raised value of the glucose-Insulin Index, indicating that miracle fruit has the ability to improve Insulin sensitivity. The plasma glucose lowering action of tolbutamide, induced by secretion of endogenous Insulin, is widely used to characterize the formation of Insulin resistance. The time for the loss of the plasma glucose lowering response to tolbutamide (10.0 mg/kg, i.p.) in fructose-rich chow fed rats was markedly delayed after treatment with miracle fruit compared with the vehicle-treated group. Thus providing supportive data that oral administration of miracle fruit could delay the development of Insulin resistance in rats. Also, the in vivo Insulin sensitivity was markedly raised by miracle fruit. In conclusion, the results suggest that miracle fruit may be used as an adjuvant for treating diabetic patients with Insulin resistance because this fruit has the ability to improve Insulin sensitivity.

  • Improvement of Insulin resistance by Hon-Chi in fructose-rich chow-fed rats
    Food Chemistry, 2020
    Co-Authors: Chih-fen Su, Juei-tang Cheng
    Abstract:

    Abstract In an attempt to develop new substances for handling Insulin resistance, the effect Hon-Chi was examined on Insulin resistance induced by fructose-rich chow in rats. Mandarin Hon-Chi is red yeast rice fermented with Monascus pilous and Monascus purpureus . Single oral administration of Hon-Chi for 90 min decreased the plasma glucose in a dose-dependent manner in rats, which had received four-week fructose-rich chow. The Insulin action on glucose disposal rate using the glucose–Insulin Index, and the value of the areas under the curve of glucose and Insulin during the intraperitoneal glucose tolerance test were measured. Oral administration (three times daily for three-days) of Hon-Chi into rats, which received four-week fructose-rich chow, reversed the elevated value of glucose-Insulin Index, indicating Hon-Chi has an ability to improve Insulin resistance. The time for the loss of plasma glucose lowering response to tolbutamide in fructose-rich chow-fed rats was markedly delayed by the repeated treatment of Hon-Chi, as compared to the vehicle-treated group. This provided the supportive data that oral administration of Hon-Chi could delay the development of Insulin resistance in rats. Increase of Insulin sensitivity by Hon-Chi was further identified using the plasma glucose lowering action of exogenous Insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Oral administration of Hon-Chi at 150 mg/kg three times daily into STZ-diabetic rats caused an increase in the responses to exogenous Insulin 15-days later. The obtained results suggest that oral administration of Hon-Chi has the ability to improve Insulin sensitivity and delay the development of Insulin resistance in rats, which may be used as an adjuvant therapy to patients with Insulin resistance.

  • Glucosamine-induced Insulin resistance in ovariectomized rats is relevant to decreasing the expression of glucose transport protein subtype 4 in the skeletal muscle and in increasing the size of pancreatic islets
    Menopause, 2012
    Co-Authors: Lin Kang, Chiung Hsin Chang, Chung Ta Lee, Chung-hwan Chen, Je-ken Chang, Juei-tang Cheng, Yueh-chin Cheng, Fong-ming Chang
    Abstract:

    OBJECTIVE: Glucosamine (GlcN) is a popular nutritional supplement used to treat osteoarthritis in postmenopausal women. Postmenopausal women are at higher risk of type 2 diabetes mellitus and metabolic syndrome because of ovarian hormone deficiency. We used ovariectomized (OVX) rats as the model to investigate whether GlcN would induce Insulin resistance (IR) in OVX rats and the underlying mechanisms. METHODS: The rats were divided into four groups: (1) sham-operated group (SHAM), (2) SHAM with GlcN treatment (SHAM + GlcN), (3) OVX group, (4) OVX with GlcN treatment (OVX + GlcN). Intraperitoneal (IP) GlcN was given at 12 weeks after the surgical procedure for 2 weeks. The IP glucose tolerance test (IPGTT) was performed to measure plasma glucose and Insulin and to calculate the clinical homeostasis model assessment-IR (HOMA-IR) and glucose-Insulin Index. Western blot analysis for the detection of glucose transport protein subtype 4 expression in the skeletal muscle and histopathological examination of the changes in pancreatic islets were also performed. RESULTS: Fasting plasma glucose increased in the OVX + GlcN group, and fasting plasma Insulin and HOMA-IR were elevated more significantly in this group. In addition, plasma glucose, plasma Insulin, HOMA-IR, and glucose-Insulin Index were significantly elevated only in the OVX with GlcN group after IP glucose injection, implying that IR was induced by GlcN only in female rats without the protection of ovarian hormone. In addition, we found that treatment with GlcN decreased the expression of glucose transport protein subtype 4 in the skeletal muscle and induced pancreatic islet hyperplasia only in OVX rats. CONCLUSIONS: The results demonstrate that female rats do not develop IR upon GlcN treatment except after ovariectomy. Those who take GlcN after menopause or bilateral oophorectomy should watch their blood glucose level closely, especially after meals.

  • Improvement of Insulin Resistance by Chlorella in Fructose‐rich Chow‐fed Rats
    Phytotherapy Research, 2011
    Co-Authors: Yi-jui Chiu, Juei-tang Cheng, H. H. Chung, Shih-hsiang Lo
    Abstract:

    Chlorella is a type of unicellular fresh water algae. In an attempt to develop new agents for handling Insulin resistance, Chlorella was employed to screen the effect on Insulin resistance in rats induced by fructose-rich chow. A single oral administration of Chlorella for 90 min decreased the plasma glucose in a dose-dependent manner in rats receiving 4-week fructose-rich chow. In addition, chronic treatment with Chlorella for 15 days also lowered plasma glucose in the same manner. Then, the Insulin action on glucose disposal rate was measured using the glucose-Insulin Index, values of the areas under the curves of glucose and Insulin during the intraperitoneal glucose tolerance test (IPGTT). Oral administration (three times daily for 5 days) of Chlorella to rats receiving 4 weeks of fructose-rich chow abolished the elevated value of the glucose-Insulin Index, indicating that Chlorella has an ability to improve Insulin resistance. An increase of Insulin sensitivity by Chlorella was further evaluated using the plasma glucose lowering action of exogenous Insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Oral administration of Chlorella three times daily to STZ-diabetic rats increased the response to exogenous Insulin 15 days later. The obtained results suggest that oral administration of Chlorella has the ability to improve Insulin sensitivity, which may be used as an adjuvant therapy for patients with Insulin resistance. Copyright © 2011 John Wiley & Sons, Ltd.

  • Merit of Ginseng in the Improvement of Insulin Resistance
    Journal of Ginseng Research, 2010
    Co-Authors: Juei-tang Cheng
    Abstract:

    In the present review, the merit of ginseng in the improvement of Insulin resistance has been introduced. Using the results in previous studies, we found that ginseng or ginsenoside Rh2 has the ability to reduce glucose-Insulin Index in rats with Insulin resistance. Insulin resistance was induced by feeding of fructose-rich chow in rats. Insulin resistance was characterized by regular methods. Effectiveness of ginseng powder or extract Rh2 was identified in this animal model. Also, the application of ginseng for handling of diabetic disorders in China has been discussed. According to Chinese traditional medicine, ginseng is merit in the treatment of diabetic disorders named as Shiaw-Ker in Chinese. Therefore, it is no doubt that ginseng is helpful in the control of diabetic disorders either prevention or the treatment. Otherwise, the potential effect of ginseng on nervous functions shall be investigated in the future.

Walter C Willett - One of the best experts on this subject based on the ideXlab platform.

  • Development and validation of empirical indices of dietary Insulinemic potential
    The FASEB Journal, 2016
    Co-Authors: Fred K. Tabung, Walter C Willett, Frank B Hu, Weike Wang, Teresa T. Fung, Stephanie A. Smith-warner, Jorge E. Chavarro, Edward Giovannucci
    Abstract:

    The glycemic Index and Insulin Index assess postprandial glycemic and Insulin response to foods, respectively, which may not reflect long-term effects of diet on glycemia or Insulinemia. We develop...

  • Adolescent and early adulthood dietary carbohydrate quantity and quality in relation to breast cancer risk
    Cancer Epidemiology Biomarkers & Prevention, 2015
    Co-Authors: Maryam S. Farvid, A. Heather Eliassen, Wendy Y. Chen, Walter C Willett
    Abstract:

    Background: We investigated quantity and quality of dietary carbohydrate as well as Insulin load and Insulin Index during adolescence and also early adulthood in relation to risk of breast cancer in the Nurses’ Health Study II. Methods: During 20 years of follow-up of 90,534 premenopausal women who completed a diet questionnaire in 1991, 2,833 invasive breast cancer cases were documented. In 1998, 44,263 of these women also completed a questionnaire about their diet during high school; among these women, we documented 1,118 cases of breast cancer. Multivariable-adjusted Cox proportional hazards regression was used to model relative risks (RR) and 95% confidence intervals (95% CI) for breast cancer across categories of dietary carbohydrate, glycemic Index (GI), glycemic load (GL), as well as Insulin load and Insulin Index scores. Results: Adolescent or early adult intakes of GI or GL were not associated with risk of breast cancer. Comparing women in the highest versus lowest quintile, the multivariable-adjusted RRs were 1.14 (0.95–1.38) for adolescent GI scores and 1.03 (0.91–1.16) for early adulthood GI scores. We also did not observe associations with Insulin Index and Insulin load scores in adolescence or early adulthood and breast cancer risk. Conclusions: We found that diets high in GI, GL, Insulin Index, and Insulin load during adolescence or early adulthood were not associated with an increased risk of breast cancer in this cohort study. Impact: Diets with a high glucose or Insulin response in adolescence or early adulthood were not significant predictors of breast cancer incidence. Cancer Epidemiol Biomarkers Prev; 24(7); 1–10. ©2015 AACR.

  • abstract p317 association of dietary Insulin Index Insulin load with risk of coronary heart disease among us men and women
    Circulation, 2015
    Co-Authors: Shanshan Li, Eric B Rimm, Frank B Hu, Laura Sampson, Mary Franz, Walter C Willett
    Abstract:

    Introduction: Dietary Insulin Index and Insulin load were developed to quantify the Insulinogenice effects of various foods to capture the postprandial Insulin response elicited by carbohydrate, protein and fat intake. However, the association between dietary Insulin Index, dietary Insulin load with risk of coronary heart disease is unknown. Methods: Based on the Nurses’ Health Study (NHS) and the Health Professionals Follow-up Study (HPFS), two large prospective cohort studies of US women and men, we included 76,277 women and 42,689 men into our study with dietary information measured every 4 years. We excluded participants with a baseline history of cardiovascular disease, type 2 diabetes, or cancer. Multivariate Cox proportional hazard models were used, adjusting for major risk factors for coronary heart diseases. We modeled dietary Insulin Index and Insulin load using simple update, cumulative average, continue updating and stop updating after intermediate outcomes. Results: The multivariate adjusted ...

  • dietary Insulin load dietary Insulin Index and risk of pancreatic cancer
    The American Journal of Clinical Nutrition, 2011
    Co-Authors: Katharina Nimptsch, Dominique S Michaud, Jennie Brandmiller, Walter C Willett, Edward Giovannucci, Brian M Wolpin, Charles S Fuchs
    Abstract:

    Background: Although hyperInsulinemia and Insulin resistance have been hypothesized to be involved in pancreatic carcinogenesis, studies that have examined glycemic load or individual dietary components that influence glucose concentrations yielded inconclusive results. Objective: Our objective was to investigate whether dietary Insulin load and dietary Insulin Index are associated with the risk of pancreatic cancer. Design: We prospectively followed 86,740 women and 46,147 men who were free of cancer and diabetes at baseline in the Nurses’ Health Study and the Health Professionals Follow-Up Study. During � 26 y of follow-up, 691 pancreatic cancer cases were documented. Dietary Insulin load was calculated as a function of the food Insulin Index, and the energy content of individual foods was reported on food-frequency questionnaires. The dietary Insulin Index was calculated by dividing the dietary Insulin load by the total energy intake. Results: Dietary Insulin load and dietary Insulin Index were not associated with the overall risk of pancreatic cancer. In a comparison of the highest with the lowest quintiles, the pooled multivariate RRs of pancreatic cancer were 1.05 (95% CI: 0.82, 1.34) for dietary Insulin load and 0.96 (95% CI: 0.75, 1.23) for dietary Insulin Index. In individuals with an elevated BMI (in kg/m 2 ; � 27.5) or with low physical activity, a high Insulin load was associated with small, nonsignificant increases in the risk of pancreatic cancer; in a comparison of the highest with the lowest tertile of intake, the positive association became more apparent in those who were both overweight and inactive (RR: 2.03; 95% CI: 1.05, 3.93; P-trend = 0.04). Conclusions: A diet that induces an elevated postprandial Insulin response does not influence the overall risk of pancreatic cancer. However, a diet with a high Insulin load may increase the risk in individuals with a preexisting state of Insulin resistance. Am J Clin Nutr 2011;94:862‐8.

  • dietary Insulin Index and Insulin load in relation to biomarkers of glycemic control plasma lipids and inflammation markers
    The American Journal of Clinical Nutrition, 2011
    Co-Authors: Katharina Nimptsch, Jennie Brandmiller, Walter C Willett, Laura Sampson, Mary Franz, Edward Giovannucci
    Abstract:

    Background: Dietary glycemic Index and load are widely used to estimate the effect of carbohydrate-containing foods on postprandial blood glucose concentrations and as surrogates for Insulin response. The food Insulin Index (II) directly quantifies the postprandial Insulin secretion of a food and takes into account foods with a low or no carbohydrate content. Objective: We investigated the average dietary II and Insulin load (IL) in relation to biomarkers of glycemic control, plasma lipids, and inflammation markers. Design: In a cross-sectional setting and with the use of data from the Nurses’ Health Study and the Health Professionals Follow-Up Study, we measured plasma concentrations of C-peptide, glycated hemoglobin (Hb A1c), HDL cholesterol, LDL cholesterol, triglycerides, C-reactive protein (CRP), and interleukin-6 (IL-6) in fasting blood samples of 4002 healthy men and women. The dietary II and IL were assessed from food-frequency questionnaires by using directly analyzed or published food II data. Results: After multivariate adjustment, participants in the highest quintile of II had 26% higher triglyceride concentrations than did participants in the lowest quintile of II (P for trend < 0.0001). This association was strongest in obese [body mass Index (in kg/m2) ≥30] participants (difference between highest and lowest quintiles in the II: 72%; P for trend = 0.01). Dietary II was inversely associated with HDL cholesterol in obese participants (difference: −18%; P for trend = 0.03). Similar associations were seen for the IL. Dietary II and IL were not significantly associated with plasma C-peptide, Hb A1c, LDL cholesterol, CRP, or IL-6. Conclusion: Dietary II and IL were not associated with fasting biomarkers of glycemic control but may be physiologically relevant to plasma lipids, especially in obese individuals.

Katharina Nimptsch - One of the best experts on this subject based on the ideXlab platform.

  • Influence of dietary Insulin scores on survival in colorectal cancer patients.
    British Journal of Cancer, 2017
    Co-Authors: Chen Yuan, J C Brand-miller, Katharina Nimptsch, Kaori Sato, Mingyang Song, Vicente Morales-oyarvide, Emilie S Zoltick, Nana Keum, Brian M Wolpin
    Abstract:

    BACKGROUND:Although hyperInsulinemia is hypothesised to be involved in colorectal carcinogenesis, it remains unclear whether a diet inducing an elevated Insulin response influences colorectal cancer (CRC) survival. METHODS:We examined the association of post-diagnosis dietary Insulin scores with survival among 2006 patients from two large prospective cohorts who were diagnosed with CRC from 1976 to 2010. Dietary Insulin load was calculated as a function of the food Insulin Index. Dietary Insulin Index was calculated by dividing Insulin load by total energy intake. Cox proportional hazards models were used to calculate hazard ratios (HRs) for CRC-specific mortality and overall mortality, adjusted for other risk factors for cancer survival. RESULTS:The adjusted HRs for CRC-specific mortality comparing the highest to the lowest quintiles were 1.82 (95% CI: 1.20-2.75, Ptrend=0.006) for dietary Insulin load and 1.66 (95% CI: 1.10-2.50, Ptrend=0.004) for dietary Insulin Index. We also observed an increased risk for overall mortality, with adjusted HRs of 1.33 (95% CI: 1.03-1.72, Ptrend=0.03) for dietary Insulin load and 1.32 (95% CI: 1.02-1.71, Ptrend=0.02) for dietary Insulin Index, comparing extreme quintiles. The increase in CRC-specific mortality associated with higher dietary Insulin scores was more apparent among patients with body mass Index (BMI)⩾25 kg m-2 than BMI

  • dietary Insulin load dietary Insulin Index and risk of pancreatic cancer
    The American Journal of Clinical Nutrition, 2011
    Co-Authors: Katharina Nimptsch, Dominique S Michaud, Jennie Brandmiller, Walter C Willett, Edward Giovannucci, Brian M Wolpin, Charles S Fuchs
    Abstract:

    Background: Although hyperInsulinemia and Insulin resistance have been hypothesized to be involved in pancreatic carcinogenesis, studies that have examined glycemic load or individual dietary components that influence glucose concentrations yielded inconclusive results. Objective: Our objective was to investigate whether dietary Insulin load and dietary Insulin Index are associated with the risk of pancreatic cancer. Design: We prospectively followed 86,740 women and 46,147 men who were free of cancer and diabetes at baseline in the Nurses’ Health Study and the Health Professionals Follow-Up Study. During � 26 y of follow-up, 691 pancreatic cancer cases were documented. Dietary Insulin load was calculated as a function of the food Insulin Index, and the energy content of individual foods was reported on food-frequency questionnaires. The dietary Insulin Index was calculated by dividing the dietary Insulin load by the total energy intake. Results: Dietary Insulin load and dietary Insulin Index were not associated with the overall risk of pancreatic cancer. In a comparison of the highest with the lowest quintiles, the pooled multivariate RRs of pancreatic cancer were 1.05 (95% CI: 0.82, 1.34) for dietary Insulin load and 0.96 (95% CI: 0.75, 1.23) for dietary Insulin Index. In individuals with an elevated BMI (in kg/m 2 ; � 27.5) or with low physical activity, a high Insulin load was associated with small, nonsignificant increases in the risk of pancreatic cancer; in a comparison of the highest with the lowest tertile of intake, the positive association became more apparent in those who were both overweight and inactive (RR: 2.03; 95% CI: 1.05, 3.93; P-trend = 0.04). Conclusions: A diet that induces an elevated postprandial Insulin response does not influence the overall risk of pancreatic cancer. However, a diet with a high Insulin load may increase the risk in individuals with a preexisting state of Insulin resistance. Am J Clin Nutr 2011;94:862‐8.

  • dietary Insulin Index and Insulin load in relation to biomarkers of glycemic control plasma lipids and inflammation markers
    The American Journal of Clinical Nutrition, 2011
    Co-Authors: Katharina Nimptsch, Jennie Brandmiller, Walter C Willett, Laura Sampson, Mary Franz, Edward Giovannucci
    Abstract:

    Background: Dietary glycemic Index and load are widely used to estimate the effect of carbohydrate-containing foods on postprandial blood glucose concentrations and as surrogates for Insulin response. The food Insulin Index (II) directly quantifies the postprandial Insulin secretion of a food and takes into account foods with a low or no carbohydrate content. Objective: We investigated the average dietary II and Insulin load (IL) in relation to biomarkers of glycemic control, plasma lipids, and inflammation markers. Design: In a cross-sectional setting and with the use of data from the Nurses’ Health Study and the Health Professionals Follow-Up Study, we measured plasma concentrations of C-peptide, glycated hemoglobin (Hb A1c), HDL cholesterol, LDL cholesterol, triglycerides, C-reactive protein (CRP), and interleukin-6 (IL-6) in fasting blood samples of 4002 healthy men and women. The dietary II and IL were assessed from food-frequency questionnaires by using directly analyzed or published food II data. Results: After multivariate adjustment, participants in the highest quintile of II had 26% higher triglyceride concentrations than did participants in the lowest quintile of II (P for trend < 0.0001). This association was strongest in obese [body mass Index (in kg/m2) ≥30] participants (difference between highest and lowest quintiles in the II: 72%; P for trend = 0.01). Dietary II was inversely associated with HDL cholesterol in obese participants (difference: −18%; P for trend = 0.03). Similar associations were seen for the IL. Dietary II and IL were not significantly associated with plasma C-peptide, Hb A1c, LDL cholesterol, CRP, or IL-6. Conclusion: Dietary II and IL were not associated with fasting biomarkers of glycemic control but may be physiologically relevant to plasma lipids, especially in obese individuals.

  • dietary glycemic Index glycemic load Insulin Index fiber and whole grain intake in relation to risk of prostate cancer
    Cancer Causes & Control, 2011
    Co-Authors: Katharina Nimptsch, Jennie Brandmiller, Mary Franz, Stacey A Kenfield, Meir J Stampfer, Majken K Jensen, L Sampson, Walter C Willett
    Abstract:

    Objective Insulin may play a role in prostate cancer tumorigenesis. Postprandial blood glucose and Insulin responses of foods depend importantly on the carbohydrate quality and quantity, represented by glycemic Index (GI), glycemic load (GL), fiber and whole-grain content, but are also influenced by intake of protein and other characteristics. The recently developed Insulin Index (II) quantifies the postprandial Insulin secretion, also taking into account these additional characteristics.

  • dietary Insulin load dietary Insulin Index and colorectal cancer
    Cancer Epidemiology Biomarkers & Prevention, 2010
    Co-Authors: Katharina Nimptsch, Jeffrey A Meyerhardt, Andrew T Chan, Kimmie Ng, Dominique S Michaud, Jennie Brandmiller, Walter C Willett, Edward Giovannucci, Charles S Fuchs
    Abstract:

    Background: Circulating Insulin levels have been positively associated with risk of colorectal cancer; however, it remains unclear whether a diet inducing an elevated Insulin response influences colorectal cancer risk. Based on a novel Insulin Index for individual foods, we estimated Insulin demand for overall diets and assessed its association with colorectal cancer in the Nurses9 Health Study and Health Professionals Follow-up Study. Methods: We followed 86,740 women and 46,146 men who were free of cancer and diabetes at baseline and identified a total of 2,481 colorectal cancer cases during up to 26 years of follow-up. Dietary Insulin load was calculated as a function of food Insulin Index and the energy content of individual foods reported on food frequency questionnaires. Average dietary Insulin Index was calculated by dividing the dietary Insulin load by the total energy intake. Results: Dietary Insulin load and dietary Insulin Index were not associated with risk of colorectal cancer. Comparing the highest with the lowest quintiles, the pooled multivariate relative risks (RRs) of colorectal cancer were 0.91 (95% confidence interval [CI] = 0.79-1.05) for dietary Insulin load and 0.93 (95% CI = 0.81-1.08) for dietary Insulin Index. Body mass Index and physical activity did not modify the association of dietary Insulin load or Index with colorectal cancer. Conclusion: A diet high in foods that increase postprandial Insulin levels did not increase risk of colorectal cancer in this large prospective study. Impact: This study is the first to investigate Insulin Index and load in relation to colorectal cancer.

Edward Giovannucci - One of the best experts on this subject based on the ideXlab platform.

  • Development and validation of empirical indices of dietary Insulinemic potential
    The FASEB Journal, 2016
    Co-Authors: Fred K. Tabung, Walter C Willett, Frank B Hu, Weike Wang, Teresa T. Fung, Stephanie A. Smith-warner, Jorge E. Chavarro, Edward Giovannucci
    Abstract:

    The glycemic Index and Insulin Index assess postprandial glycemic and Insulin response to foods, respectively, which may not reflect long-term effects of diet on glycemia or Insulinemia. We develop...

  • dietary Insulin Index and Insulin load in relation to endometrial cancer risk in the nurses health study
    Cancer Epidemiology Biomarkers & Prevention, 2014
    Co-Authors: Edward Giovannucci, Jennifer Prescott, Akila N Viswanathan, Susan E Hankinson, Immaculata De Vivo
    Abstract:

    Background: Although unopposed estrogen exposure is considered the main driver of endometrial carcinogenesis, factors associated with states of Insulin resistance and hyperInsulinemia are independently associated with endometrial cancer risk. We used dietary Insulin load and Insulin Index scores to represent the estimated Insulin demand of overall diets and assessed their association with endometrial cancer risk in the prospective Nurses' Health Study. Methods: We estimated incidence rate ratios (RR) and 95% confidence intervals (CI) for risk of invasive endometrial cancer using Cox proportional hazards models. Between the baseline dietary questionnaire (1980) and 2010, we identified a total of 798 incident-invasive epithelial endometrial adenocarcinomas over 1,417,167 person-years of follow-up. Results: Dietary Insulin scores were not associated with overall risk of endometrial cancer. Comparing women in the highest with the lowest quintile, the multivariable-adjusted RRs of endometrial cancer were 1.07 (95% CI, 0.84–1.35) for cumulative average dietary Insulin load and 1.03 (95% CI, 0.82–1.31) for cumulative average dietary Insulin Index. Findings did not vary substantially by alcohol consumption, total dietary fiber intake, or body mass Index and/or physical activity ( P heterogeneity ≥ 0.10). Conclusions: Intake of a diet predicted to stimulate a high postprandial Insulin response was not associated with endometrial cancer risk in this large prospective study. Considering the complex interplay of diet, lifestyle, and genetic factors contributing to the hyperInsulinemic state, dietary measures alone may not sufficiently capture absolute long-term Insulin exposure. Impact: This study is the first to investigate dietary Insulin scores in relation to endometrial cancer risk. Cancer Epidemiol Biomarkers Prev; 23(8); 1512–20. ©2014 AACR . This article is featured in Highlights of This Issue, [p. 1443][1] [1]: /lookup/volpage/23/1443?iss=8

  • dietary Insulin load dietary Insulin Index and risk of pancreatic cancer
    The American Journal of Clinical Nutrition, 2011
    Co-Authors: Katharina Nimptsch, Dominique S Michaud, Jennie Brandmiller, Walter C Willett, Edward Giovannucci, Brian M Wolpin, Charles S Fuchs
    Abstract:

    Background: Although hyperInsulinemia and Insulin resistance have been hypothesized to be involved in pancreatic carcinogenesis, studies that have examined glycemic load or individual dietary components that influence glucose concentrations yielded inconclusive results. Objective: Our objective was to investigate whether dietary Insulin load and dietary Insulin Index are associated with the risk of pancreatic cancer. Design: We prospectively followed 86,740 women and 46,147 men who were free of cancer and diabetes at baseline in the Nurses’ Health Study and the Health Professionals Follow-Up Study. During � 26 y of follow-up, 691 pancreatic cancer cases were documented. Dietary Insulin load was calculated as a function of the food Insulin Index, and the energy content of individual foods was reported on food-frequency questionnaires. The dietary Insulin Index was calculated by dividing the dietary Insulin load by the total energy intake. Results: Dietary Insulin load and dietary Insulin Index were not associated with the overall risk of pancreatic cancer. In a comparison of the highest with the lowest quintiles, the pooled multivariate RRs of pancreatic cancer were 1.05 (95% CI: 0.82, 1.34) for dietary Insulin load and 0.96 (95% CI: 0.75, 1.23) for dietary Insulin Index. In individuals with an elevated BMI (in kg/m 2 ; � 27.5) or with low physical activity, a high Insulin load was associated with small, nonsignificant increases in the risk of pancreatic cancer; in a comparison of the highest with the lowest tertile of intake, the positive association became more apparent in those who were both overweight and inactive (RR: 2.03; 95% CI: 1.05, 3.93; P-trend = 0.04). Conclusions: A diet that induces an elevated postprandial Insulin response does not influence the overall risk of pancreatic cancer. However, a diet with a high Insulin load may increase the risk in individuals with a preexisting state of Insulin resistance. Am J Clin Nutr 2011;94:862‐8.

  • dietary Insulin Index and Insulin load in relation to biomarkers of glycemic control plasma lipids and inflammation markers
    The American Journal of Clinical Nutrition, 2011
    Co-Authors: Katharina Nimptsch, Jennie Brandmiller, Walter C Willett, Laura Sampson, Mary Franz, Edward Giovannucci
    Abstract:

    Background: Dietary glycemic Index and load are widely used to estimate the effect of carbohydrate-containing foods on postprandial blood glucose concentrations and as surrogates for Insulin response. The food Insulin Index (II) directly quantifies the postprandial Insulin secretion of a food and takes into account foods with a low or no carbohydrate content. Objective: We investigated the average dietary II and Insulin load (IL) in relation to biomarkers of glycemic control, plasma lipids, and inflammation markers. Design: In a cross-sectional setting and with the use of data from the Nurses’ Health Study and the Health Professionals Follow-Up Study, we measured plasma concentrations of C-peptide, glycated hemoglobin (Hb A1c), HDL cholesterol, LDL cholesterol, triglycerides, C-reactive protein (CRP), and interleukin-6 (IL-6) in fasting blood samples of 4002 healthy men and women. The dietary II and IL were assessed from food-frequency questionnaires by using directly analyzed or published food II data. Results: After multivariate adjustment, participants in the highest quintile of II had 26% higher triglyceride concentrations than did participants in the lowest quintile of II (P for trend < 0.0001). This association was strongest in obese [body mass Index (in kg/m2) ≥30] participants (difference between highest and lowest quintiles in the II: 72%; P for trend = 0.01). Dietary II was inversely associated with HDL cholesterol in obese participants (difference: −18%; P for trend = 0.03). Similar associations were seen for the IL. Dietary II and IL were not significantly associated with plasma C-peptide, Hb A1c, LDL cholesterol, CRP, or IL-6. Conclusion: Dietary II and IL were not associated with fasting biomarkers of glycemic control but may be physiologically relevant to plasma lipids, especially in obese individuals.

  • dietary Insulin load dietary Insulin Index and colorectal cancer
    Cancer Epidemiology Biomarkers & Prevention, 2010
    Co-Authors: Katharina Nimptsch, Jeffrey A Meyerhardt, Andrew T Chan, Kimmie Ng, Dominique S Michaud, Jennie Brandmiller, Walter C Willett, Edward Giovannucci, Charles S Fuchs
    Abstract:

    Background: Circulating Insulin levels have been positively associated with risk of colorectal cancer; however, it remains unclear whether a diet inducing an elevated Insulin response influences colorectal cancer risk. Based on a novel Insulin Index for individual foods, we estimated Insulin demand for overall diets and assessed its association with colorectal cancer in the Nurses9 Health Study and Health Professionals Follow-up Study. Methods: We followed 86,740 women and 46,146 men who were free of cancer and diabetes at baseline and identified a total of 2,481 colorectal cancer cases during up to 26 years of follow-up. Dietary Insulin load was calculated as a function of food Insulin Index and the energy content of individual foods reported on food frequency questionnaires. Average dietary Insulin Index was calculated by dividing the dietary Insulin load by the total energy intake. Results: Dietary Insulin load and dietary Insulin Index were not associated with risk of colorectal cancer. Comparing the highest with the lowest quintiles, the pooled multivariate relative risks (RRs) of colorectal cancer were 0.91 (95% confidence interval [CI] = 0.79-1.05) for dietary Insulin load and 0.93 (95% CI = 0.81-1.08) for dietary Insulin Index. Body mass Index and physical activity did not modify the association of dietary Insulin load or Index with colorectal cancer. Conclusion: A diet high in foods that increase postprandial Insulin levels did not increase risk of colorectal cancer in this large prospective study. Impact: This study is the first to investigate Insulin Index and load in relation to colorectal cancer.

Jennie Brandmiller - One of the best experts on this subject based on the ideXlab platform.

  • dietary Insulin load dietary Insulin Index and risk of pancreatic cancer
    The American Journal of Clinical Nutrition, 2011
    Co-Authors: Katharina Nimptsch, Dominique S Michaud, Jennie Brandmiller, Walter C Willett, Edward Giovannucci, Brian M Wolpin, Charles S Fuchs
    Abstract:

    Background: Although hyperInsulinemia and Insulin resistance have been hypothesized to be involved in pancreatic carcinogenesis, studies that have examined glycemic load or individual dietary components that influence glucose concentrations yielded inconclusive results. Objective: Our objective was to investigate whether dietary Insulin load and dietary Insulin Index are associated with the risk of pancreatic cancer. Design: We prospectively followed 86,740 women and 46,147 men who were free of cancer and diabetes at baseline in the Nurses’ Health Study and the Health Professionals Follow-Up Study. During � 26 y of follow-up, 691 pancreatic cancer cases were documented. Dietary Insulin load was calculated as a function of the food Insulin Index, and the energy content of individual foods was reported on food-frequency questionnaires. The dietary Insulin Index was calculated by dividing the dietary Insulin load by the total energy intake. Results: Dietary Insulin load and dietary Insulin Index were not associated with the overall risk of pancreatic cancer. In a comparison of the highest with the lowest quintiles, the pooled multivariate RRs of pancreatic cancer were 1.05 (95% CI: 0.82, 1.34) for dietary Insulin load and 0.96 (95% CI: 0.75, 1.23) for dietary Insulin Index. In individuals with an elevated BMI (in kg/m 2 ; � 27.5) or with low physical activity, a high Insulin load was associated with small, nonsignificant increases in the risk of pancreatic cancer; in a comparison of the highest with the lowest tertile of intake, the positive association became more apparent in those who were both overweight and inactive (RR: 2.03; 95% CI: 1.05, 3.93; P-trend = 0.04). Conclusions: A diet that induces an elevated postprandial Insulin response does not influence the overall risk of pancreatic cancer. However, a diet with a high Insulin load may increase the risk in individuals with a preexisting state of Insulin resistance. Am J Clin Nutr 2011;94:862‐8.

  • dietary Insulin Index and Insulin load in relation to biomarkers of glycemic control plasma lipids and inflammation markers
    The American Journal of Clinical Nutrition, 2011
    Co-Authors: Katharina Nimptsch, Jennie Brandmiller, Walter C Willett, Laura Sampson, Mary Franz, Edward Giovannucci
    Abstract:

    Background: Dietary glycemic Index and load are widely used to estimate the effect of carbohydrate-containing foods on postprandial blood glucose concentrations and as surrogates for Insulin response. The food Insulin Index (II) directly quantifies the postprandial Insulin secretion of a food and takes into account foods with a low or no carbohydrate content. Objective: We investigated the average dietary II and Insulin load (IL) in relation to biomarkers of glycemic control, plasma lipids, and inflammation markers. Design: In a cross-sectional setting and with the use of data from the Nurses’ Health Study and the Health Professionals Follow-Up Study, we measured plasma concentrations of C-peptide, glycated hemoglobin (Hb A1c), HDL cholesterol, LDL cholesterol, triglycerides, C-reactive protein (CRP), and interleukin-6 (IL-6) in fasting blood samples of 4002 healthy men and women. The dietary II and IL were assessed from food-frequency questionnaires by using directly analyzed or published food II data. Results: After multivariate adjustment, participants in the highest quintile of II had 26% higher triglyceride concentrations than did participants in the lowest quintile of II (P for trend < 0.0001). This association was strongest in obese [body mass Index (in kg/m2) ≥30] participants (difference between highest and lowest quintiles in the II: 72%; P for trend = 0.01). Dietary II was inversely associated with HDL cholesterol in obese participants (difference: −18%; P for trend = 0.03). Similar associations were seen for the IL. Dietary II and IL were not significantly associated with plasma C-peptide, Hb A1c, LDL cholesterol, CRP, or IL-6. Conclusion: Dietary II and IL were not associated with fasting biomarkers of glycemic control but may be physiologically relevant to plasma lipids, especially in obese individuals.

  • dietary glycemic Index glycemic load Insulin Index fiber and whole grain intake in relation to risk of prostate cancer
    Cancer Causes & Control, 2011
    Co-Authors: Katharina Nimptsch, Jennie Brandmiller, Mary Franz, Stacey A Kenfield, Meir J Stampfer, Majken K Jensen, L Sampson, Walter C Willett
    Abstract:

    Objective Insulin may play a role in prostate cancer tumorigenesis. Postprandial blood glucose and Insulin responses of foods depend importantly on the carbohydrate quality and quantity, represented by glycemic Index (GI), glycemic load (GL), fiber and whole-grain content, but are also influenced by intake of protein and other characteristics. The recently developed Insulin Index (II) quantifies the postprandial Insulin secretion, also taking into account these additional characteristics.

  • dietary Insulin load dietary Insulin Index and colorectal cancer
    Cancer Epidemiology Biomarkers & Prevention, 2010
    Co-Authors: Katharina Nimptsch, Jeffrey A Meyerhardt, Andrew T Chan, Kimmie Ng, Dominique S Michaud, Jennie Brandmiller, Walter C Willett, Edward Giovannucci, Charles S Fuchs
    Abstract:

    Background: Circulating Insulin levels have been positively associated with risk of colorectal cancer; however, it remains unclear whether a diet inducing an elevated Insulin response influences colorectal cancer risk. Based on a novel Insulin Index for individual foods, we estimated Insulin demand for overall diets and assessed its association with colorectal cancer in the Nurses9 Health Study and Health Professionals Follow-up Study. Methods: We followed 86,740 women and 46,146 men who were free of cancer and diabetes at baseline and identified a total of 2,481 colorectal cancer cases during up to 26 years of follow-up. Dietary Insulin load was calculated as a function of food Insulin Index and the energy content of individual foods reported on food frequency questionnaires. Average dietary Insulin Index was calculated by dividing the dietary Insulin load by the total energy intake. Results: Dietary Insulin load and dietary Insulin Index were not associated with risk of colorectal cancer. Comparing the highest with the lowest quintiles, the pooled multivariate relative risks (RRs) of colorectal cancer were 0.91 (95% confidence interval [CI] = 0.79-1.05) for dietary Insulin load and 0.93 (95% CI = 0.81-1.08) for dietary Insulin Index. Body mass Index and physical activity did not modify the association of dietary Insulin load or Index with colorectal cancer. Conclusion: A diet high in foods that increase postprandial Insulin levels did not increase risk of colorectal cancer in this large prospective study. Impact: This study is the first to investigate Insulin Index and load in relation to colorectal cancer.

  • abstract 2823 dietary glycemic Index glycemic load and Insulin Index in relation to risk of prostate cancer
    Cancer Research, 2010
    Co-Authors: Katharina Nimptsch, Jennie Brandmiller, Walter C Willett, Laura Sampson, Mary Franz, Stacey A Kenfield, Meir J Stampfer, Edward Giovannucci
    Abstract:

    Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC Background: The Insulin and Insulin-like growth factor (IGF) axis has been shown to play a role in prostate cancer tumorigenesis. Circulating IGF-1 and fasting Insulin as well as Insulin resistance have been associated with increased risk of total or advanced prostate cancer in some epidemiological studies. Through alterations by diet the Insulin and IGF axis may be potentially modifiable. The dietary Insulin response depends largely but not entirely on the quality and quantity of dietary carbohydrates. The glycemic Index (GI) is a measure of the propensity of carbohydrate containing foods to raise blood glucose levels postprandially. The more recently developed food Insulin Index is a comparable measure which is based on the diet's effect on Insulin secretion, also taking into account foods with low or no carbohydrate content. We hypothesized that high dietary glycemic Index, glycemic load (GL) and Insulin Index (II) are associated with increased risk of prostate cancer. Material and Methods: We followed 47,779 Health Professionals Follow-up Study participants between 1986 and 2006 for prostate cancer incidence. Dietary intake was assessed by food frequency questionnaire (FFQ) in 1986 and updated every 4 years. Dietary GL was calculated by multiplying GI by the carbohydrate content and consumption frequency of each FFQ item and then summing over all the items. Values for the food Insulin Index of the FFQ items were provided by the University of Sydney, Australia. The dietary II was calculated as a function of food Insulin Index, energy content and consumption frequency of all FFQ items. Multivariate adjusted hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox proportional hazards regression. Results: Between 1986 and 2006, we confirmed 5,112 prostate cancer cases, including 860 advanced/fatal (regionally invasive or metastatic disease at diagnosis, or metastases or death from prostate cancer during follow-up) cases. Dietary GI, GL and II were not associated with risk of total or advanced prostate cancer. For total prostate cancer, the multivariate adjusted HRs comparing the highest versus lowest quintile were 1.01 (CI 0.92-1.12, p-trend=0.26) for GI, 1.07 (CI 0.97-1.19, p-trend=0.19) for GL and 1.05 (CI 0.94-1.17, p-trend=0.15) for II. For advanced prostate cancer, the HRs were 1.05 (CI 0.75-1.47, p-trend=0.76) for GI, 0.99 (CI 0.70-1.40, p-trend=0.64) for GL, and 0.99 (CI 0.68-1.44, p-trend=0.92) for II. Results did not change substantially when the cohort was restricted to men with PSA screening. Stratification by BMI, diabetes and age at diagnosis, or by tumor grade, did not suggest any heterogeneity (all p-values for interaction were >0.11). Conclusion: These results suggest that long-term exposure to a diet with a high Insulin response as reflected by high dietary glycemic Index, glycemic load and Insulin Index does not affect prostate cancer incidence or progression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2823.