The Experts below are selected from a list of 5568 Experts worldwide ranked by ideXlab platform
Richard S. Bruno - One of the best experts on this subject based on the ideXlab platform.
-
supplementation of a γ tocopherol rich mixture of tocopherols in healthy men protects against vascular endothelial dysfunction induced by Postprandial Hyperglycemia
Journal of Nutritional Biochemistry, 2013Co-Authors: Eunice Mah, Sang K. Noh, Kevin D. Ballard, Jeff S. Volek, Hea Jin Park, Richard S. BrunoAbstract:Postprandial Hyperglycemia induces oxidative stress responses, impairs vascular endothelial function (VEF) and increases the risk of cardiovascular disease. We hypothesized that the antioxidant and anti-inflammatory activities of a γ-tocopherol-rich mixture of tocopherols (γ-TmT) would protect against vascular dysfunction that is otherwise caused by Postprandial Hyperglycemia by decreasing oxidative stress and proinflammatory responses, and improving nitric oxide (NO•) homeostasis. In a randomized, crossover study, healthy men (n=15; 21.8 ± 0.8 years) completed a fasting oral glucose challenge (75 g) with or without prior supplementation of γ-TmT (5 days). Brachial artery flow-mediated dilation (FMD), plasma glucose, insulin, antioxidants, malondialdehyde (MDA), inflammatory proteins, arginine and asymmetric dimethylarginine (ADMA) were measured at regular intervals during a 3-h Postprandial period. Supplementation of γ-TmT increased (P .05). Postprandial FMD decreased 30%-44% (P<.05) following glucose ingestion, but was maintained with γ-TmT. Supplementation of γ-TmT also attenuated Postprandial increases in MDA that occurred following glucose ingestion. Plasma arginine decreased (P<.05) in both trials to a similar extent regardless of γ-TmT supplementation. However, the ratio of ADMA/arginine increased time-dependently in both trials (P<.05), but to a lesser extent following γ-TmT supplementation (P<.05). Inflammatory proteins were unaffected by glucose ingestion or γ-TmT. Collectively, these findings support that short-term supplementation of γ-TmT maintains VEF during Postprandial Hyperglycemia possibly by attenuating lipid peroxidation and disruptions in NO• homeostasis, independent of inflammation.
-
Postprandial Hyperglycemia on vascular endothelial function: mechanisms and consequences
Nutrition research (New York N.Y.), 2012Co-Authors: Eunice Mah, Richard S. BrunoAbstract:Abstract Vascular endothelial dysfunction precedes atherosclerosis and contributes to cardiovascular disease (CVD), which accounts for one-third of all deaths in the United States. Chronic Hyperglycemia, such as that associated with diabetes, is well known to impair vascular function. However, recent evidence demonstrates that acute or Postprandial Hyperglycemia (PPH) not only exacerbates vascular endothelial dysfunction in individuals with chronic Hyperglycemia but also transiently impairs vascular function in healthy individuals. Postprandial Hyperglycemia has been shown to better predict future CVD mortality compared with fasting glucose in both diabetic and normoglycemic individuals. Compelling evidence exists suggesting that PPH-mediated insults to the vascular endothelium contribute to CVD, especially in pathophysiologic conditions whereby vascular recovery is compromised. Although the mechanisms by which PPH induces vascular dysfunction is not fully understood, oxidative stress–mediated disruptions in nitric oxide homeostasis are implicated as key events leading to vascular dysfunction associated with PPH. This review aims to highlight the findings of clinical studies using functional indices of vascular function to demonstrate that PPH impairs vascular function. We will also discuss the evidence showing the central involvement of oxidative stress in dysregulating nitric oxide homeostasis and contributing to PPH-mediated vascular endothelial dysfunction. Lastly, this review will identify areas of knowledge that remain limited and will provide recommendations for future investigation to more fully define PPH as an important risk factor for CVD.
-
Supplementation of a γ-tocopherol-rich mixture of tocopherols in healthy men protects against vascular endothelial dysfunction induced by Postprandial Hyperglycemia.
The Journal of nutritional biochemistry, 2012Co-Authors: Eunice Mah, Sang K. Noh, Kevin D. Ballard, Jeff S. Volek, Hea Jin Park, Richard S. BrunoAbstract:Postprandial Hyperglycemia induces oxidative stress responses, impairs vascular endothelial function (VEF) and increases the risk of cardiovascular disease. We hypothesized that the antioxidant and anti-inflammatory activities of a γ-tocopherol-rich mixture of tocopherols (γ-TmT) would protect against vascular dysfunction that is otherwise caused by Postprandial Hyperglycemia by decreasing oxidative stress and proinflammatory responses, and improving nitric oxide (NO•) homeostasis. In a randomized, crossover study, healthy men (n=15; 21.8 ± 0.8 years) completed a fasting oral glucose challenge (75 g) with or without prior supplementation of γ-TmT (5 days). Brachial artery flow-mediated dilation (FMD), plasma glucose, insulin, antioxidants, malondialdehyde (MDA), inflammatory proteins, arginine and asymmetric dimethylarginine (ADMA) were measured at regular intervals during a 3-h Postprandial period. Supplementation of γ-TmT increased (P .05). Postprandial FMD decreased 30%-44% (P
-
Postprandial Hyperglycemia Impairs Vascular Endothelial Function in Healthy Men by Inducing Lipid Peroxidation and Increasing Asymmetric Dimethylarginine:Arginine
The Journal of nutrition, 2011Co-Authors: Eunice Mah, Sang K. Noh, Kevin D. Ballard, Manuel E. Matos, Jeff S. Volek, Richard S. BrunoAbstract:Postprandial Hyperglycemia induces vascular endothelial dysfunction (VED) and increases future cardiovascular disease risk. We hypothesized that Postprandial Hyperglycemia would decrease vascular function in healthy men by inducing oxidative stress and proinflammatory responses and increasing asymmetric dimethylarginine:arginine (ADMA:arginine), a biomarker that is predictive of reduced NO biosynthesis. In a randomized, cross-over design, healthy men (n = 16; 21.6 ± 0.8 y) ingested glucose or fructose (75 g) after an overnight fast. Brachial artery flow-mediated dilation (FMD), plasma glucose and insulin, antioxidants, malondialdehyde (MDA), inflammatory proteins, arginine, and ADMA were measured at regular intervals during the 3-h Postprandial period. Baseline FMD did not differ between trials (P > 0.05). Postprandial FMD was reduced following the ingestion of glucose only. Postprandial MDA concentrations increased to a greater extent following the ingestion of glucose compared to fructose. Plasma arginine decreased and the ratio of ADMA:arginine increased to a greater extent following the ingestion of glucose. Inflammatory cytokines and cellular adhesion molecules were unaffected by the ingestion of either sugar. Postprandial AUC(0-3 h) for FMD and MDA were inversely related (r = -0.80; P < 0.05), suggesting that Hyperglycemia-induced lipid peroxidation suppresses Postprandial vascular function. Collectively, these findings suggest that Postprandial Hyperglycemia in healthy men reduces endothelium-dependent vasodilation by increasing lipid peroxidation independent of inflammation. Postprandial alterations in arginine and ADMA:arginine also suggest that acute Hyperglycemia may induce VED by decreasing NO bioavailability through an oxidative stress-dependent mechanism. Additional work is warranted to define whether inhibiting lipid peroxidation and restoring arginine metabolism would mitigate Hyperglycemia-mediated decreases in vascular function.
Johji Yamahara - One of the best experts on this subject based on the ideXlab platform.
-
Punica granatum flower extract, a potent α-glucosidase inhibitor, improves Postprandial Hyperglycemia in Zucker diabetic fatty rats
Journal of ethnopharmacology, 2005Co-Authors: Suping Wen, Gang Peng, Johji Yamahara, Bhavani Prasad Kota, Basil D. RoufogalisAbstract:Postprandial Hyperglycemia plays an important role in the development of type 2 diabetes and has been proposed as an independent risk factor for cardiovascular diseases. The flowering part of Punica granatum Linn. (Punicaceae) (PGF) has been recommended in Unani literature as a remedy for diabetes. We investigated the effect and action mechanism of a methanolic extract from PGF on Hyperglycemia in vivo and in vitro. Oral administration of PGF extract markedly lowered plasma glucose levels in non-fasted Zucker diabetic fatty rats (a genetic model of obesity and type 2 diabetes), whereas it had little effect in the fasted animals, suggesting it affected Postprandial Hyperglycemia in type 2 diabetes. In support of this conclusion the extract was found to markedly inhibit the increase of plasma glucose levels after sucrose loading, but not after glucose loading in mice, and it had no effect on glucose levels in normal mice. In vitro, PGF extract demonstrated a potent inhibitory effect on alpha-glucosidase activity (IC50: 1.8 microg/ml). The inhibition is dependent on the concentration of enzyme and substrate, as well as on the length of pretreatment with the enzyme. These findings strongly suggest that PGF extract improves Postprandial Hyperglycemia in type 2 diabetes and obesity, at least in part, by inhibiting intestinal alpha-glucosidase activity.
-
Salacia oblonga improves cardiac fibrosis and inhibits Postprandial Hyperglycemia in obese Zucker rats.
Life sciences, 2004Co-Authors: Gang Peng, Li Qian, Suping Wen, Tom Hsun-wei Huang, Basil D. Roufogalis, Johji YamaharaAbstract:Diabetes has a markedly greater incidence of cardiovascular disease than the non-diabetic population. The heart shows a slowly developing increase in fibrosis in diabetes. Extended cardiac fibrosis results in increased myocardial stiffness, causing ventricular dysfunction and, ultimately, heart failure. Reversal of fibrosis may improve organ function survival. Postprandial Hyperglycemia plays an important role in the development of type 2 diabetes and cardiovascular complications, and has been proposed as an independent risk factor for cardiovascular diseases. Salacia oblonga (S.O.) is traditionally used in the prevention and treatment of diabetes. We investigated the effects of its water extract on cardiac fibrosis and Hyperglycemia in a genetic model of type 2 diabetes, the obese Zucker rat (OZR). Chronic administration of the extract markedly improved interstitial and perivascular fibrosis in the hearts of the OZR. It also reduced plasma glucose levels in non-fasted OZR, whereas it had little effect in the fasted animals, suggesting inhibition of Postprandial Hyperglycemia in type 2 diabetic animals, which might play a role in improvement of the cardiac complications of OZR. Furthermore, S.O. markedly suppressed the overexpression of mRNAs encoding transforming growth factor betas 1 and 3 in the OZR heart, which may be an important part of the overall molecular mechanisms. S.O. dose-dependently inhibited the increase of plasma glucose in sucrose-, but not in glucose-loaded mice. S.O. demonstrated a strong inhibition of alpha-glucosidase activity in vitro, which is suggested to contribute to the improvement of Postprandial Hyperglycemia.
-
salacia oblonga improves cardiac fibrosis and inhibits Postprandial Hyperglycemia in obese zucker rats
Life Sciences, 2004Co-Authors: Gang Peng, Suping Wen, Tom Hsun-wei Huang, Basil D. Roufogalis, Johji YamaharaAbstract:Diabetes has a markedly greater incidence of cardiovascular disease than the non-diabetic population. The heart shows a slowly developing increase in fibrosis in diabetes. Extended cardiac fibrosis results in increased myocardial stiffness, causing ventricular dysfunction and, ultimately, heart failure. Reversal of fibrosis may improve organ function survival. Postprandial Hyperglycemia plays an important role in the development of type 2 diabetes and cardiovascular complications, and has been proposed as an independent risk factor for cardiovascular diseases. Salacia oblonga (S.O.) is traditionally used in the prevention and treatment of diabetes. We investigated the effects of its water extract on cardiac fibrosis and Hyperglycemia in a genetic model of type 2 diabetes, the obese Zucker rat (OZR). Chronic administration of the extract markedly improved interstitial and perivascular fibrosis in the hearts of the OZR. It also reduced plasma glucose levels in non-fasted OZR, whereas it had little effect in the fasted animals, suggesting inhibition of Postprandial Hyperglycemia in type 2 diabetic animals, which might play a role in improvement of the cardiac complications of OZR. Furthermore, S.O. markedly suppressed the overexpression of mRNAs encoding transforming growth factor βs 1 and 3 in the OZR heart, which may be an important part of the overall molecular mechanisms. S.O. dose-dependently inhibited the increase of plasma glucose in sucrose-, but not in glucose-loaded mice. S.O. demonstrated a strong inhibition of α-glucosidase activity in vitro, which is suggested to contribute to the improvement of Postprandial Hyperglycemia.
Eunice Mah - One of the best experts on this subject based on the ideXlab platform.
-
supplementation of a γ tocopherol rich mixture of tocopherols in healthy men protects against vascular endothelial dysfunction induced by Postprandial Hyperglycemia
Journal of Nutritional Biochemistry, 2013Co-Authors: Eunice Mah, Sang K. Noh, Kevin D. Ballard, Jeff S. Volek, Hea Jin Park, Richard S. BrunoAbstract:Postprandial Hyperglycemia induces oxidative stress responses, impairs vascular endothelial function (VEF) and increases the risk of cardiovascular disease. We hypothesized that the antioxidant and anti-inflammatory activities of a γ-tocopherol-rich mixture of tocopherols (γ-TmT) would protect against vascular dysfunction that is otherwise caused by Postprandial Hyperglycemia by decreasing oxidative stress and proinflammatory responses, and improving nitric oxide (NO•) homeostasis. In a randomized, crossover study, healthy men (n=15; 21.8 ± 0.8 years) completed a fasting oral glucose challenge (75 g) with or without prior supplementation of γ-TmT (5 days). Brachial artery flow-mediated dilation (FMD), plasma glucose, insulin, antioxidants, malondialdehyde (MDA), inflammatory proteins, arginine and asymmetric dimethylarginine (ADMA) were measured at regular intervals during a 3-h Postprandial period. Supplementation of γ-TmT increased (P .05). Postprandial FMD decreased 30%-44% (P<.05) following glucose ingestion, but was maintained with γ-TmT. Supplementation of γ-TmT also attenuated Postprandial increases in MDA that occurred following glucose ingestion. Plasma arginine decreased (P<.05) in both trials to a similar extent regardless of γ-TmT supplementation. However, the ratio of ADMA/arginine increased time-dependently in both trials (P<.05), but to a lesser extent following γ-TmT supplementation (P<.05). Inflammatory proteins were unaffected by glucose ingestion or γ-TmT. Collectively, these findings support that short-term supplementation of γ-TmT maintains VEF during Postprandial Hyperglycemia possibly by attenuating lipid peroxidation and disruptions in NO• homeostasis, independent of inflammation.
-
Postprandial Hyperglycemia on vascular endothelial function: mechanisms and consequences
Nutrition research (New York N.Y.), 2012Co-Authors: Eunice Mah, Richard S. BrunoAbstract:Abstract Vascular endothelial dysfunction precedes atherosclerosis and contributes to cardiovascular disease (CVD), which accounts for one-third of all deaths in the United States. Chronic Hyperglycemia, such as that associated with diabetes, is well known to impair vascular function. However, recent evidence demonstrates that acute or Postprandial Hyperglycemia (PPH) not only exacerbates vascular endothelial dysfunction in individuals with chronic Hyperglycemia but also transiently impairs vascular function in healthy individuals. Postprandial Hyperglycemia has been shown to better predict future CVD mortality compared with fasting glucose in both diabetic and normoglycemic individuals. Compelling evidence exists suggesting that PPH-mediated insults to the vascular endothelium contribute to CVD, especially in pathophysiologic conditions whereby vascular recovery is compromised. Although the mechanisms by which PPH induces vascular dysfunction is not fully understood, oxidative stress–mediated disruptions in nitric oxide homeostasis are implicated as key events leading to vascular dysfunction associated with PPH. This review aims to highlight the findings of clinical studies using functional indices of vascular function to demonstrate that PPH impairs vascular function. We will also discuss the evidence showing the central involvement of oxidative stress in dysregulating nitric oxide homeostasis and contributing to PPH-mediated vascular endothelial dysfunction. Lastly, this review will identify areas of knowledge that remain limited and will provide recommendations for future investigation to more fully define PPH as an important risk factor for CVD.
-
Supplementation of a γ-tocopherol-rich mixture of tocopherols in healthy men protects against vascular endothelial dysfunction induced by Postprandial Hyperglycemia.
The Journal of nutritional biochemistry, 2012Co-Authors: Eunice Mah, Sang K. Noh, Kevin D. Ballard, Jeff S. Volek, Hea Jin Park, Richard S. BrunoAbstract:Postprandial Hyperglycemia induces oxidative stress responses, impairs vascular endothelial function (VEF) and increases the risk of cardiovascular disease. We hypothesized that the antioxidant and anti-inflammatory activities of a γ-tocopherol-rich mixture of tocopherols (γ-TmT) would protect against vascular dysfunction that is otherwise caused by Postprandial Hyperglycemia by decreasing oxidative stress and proinflammatory responses, and improving nitric oxide (NO•) homeostasis. In a randomized, crossover study, healthy men (n=15; 21.8 ± 0.8 years) completed a fasting oral glucose challenge (75 g) with or without prior supplementation of γ-TmT (5 days). Brachial artery flow-mediated dilation (FMD), plasma glucose, insulin, antioxidants, malondialdehyde (MDA), inflammatory proteins, arginine and asymmetric dimethylarginine (ADMA) were measured at regular intervals during a 3-h Postprandial period. Supplementation of γ-TmT increased (P .05). Postprandial FMD decreased 30%-44% (P
-
Postprandial Hyperglycemia Impairs Vascular Endothelial Function in Healthy Men by Inducing Lipid Peroxidation and Increasing Asymmetric Dimethylarginine:Arginine
The Journal of nutrition, 2011Co-Authors: Eunice Mah, Sang K. Noh, Kevin D. Ballard, Manuel E. Matos, Jeff S. Volek, Richard S. BrunoAbstract:Postprandial Hyperglycemia induces vascular endothelial dysfunction (VED) and increases future cardiovascular disease risk. We hypothesized that Postprandial Hyperglycemia would decrease vascular function in healthy men by inducing oxidative stress and proinflammatory responses and increasing asymmetric dimethylarginine:arginine (ADMA:arginine), a biomarker that is predictive of reduced NO biosynthesis. In a randomized, cross-over design, healthy men (n = 16; 21.6 ± 0.8 y) ingested glucose or fructose (75 g) after an overnight fast. Brachial artery flow-mediated dilation (FMD), plasma glucose and insulin, antioxidants, malondialdehyde (MDA), inflammatory proteins, arginine, and ADMA were measured at regular intervals during the 3-h Postprandial period. Baseline FMD did not differ between trials (P > 0.05). Postprandial FMD was reduced following the ingestion of glucose only. Postprandial MDA concentrations increased to a greater extent following the ingestion of glucose compared to fructose. Plasma arginine decreased and the ratio of ADMA:arginine increased to a greater extent following the ingestion of glucose. Inflammatory cytokines and cellular adhesion molecules were unaffected by the ingestion of either sugar. Postprandial AUC(0-3 h) for FMD and MDA were inversely related (r = -0.80; P < 0.05), suggesting that Hyperglycemia-induced lipid peroxidation suppresses Postprandial vascular function. Collectively, these findings suggest that Postprandial Hyperglycemia in healthy men reduces endothelium-dependent vasodilation by increasing lipid peroxidation independent of inflammation. Postprandial alterations in arginine and ADMA:arginine also suggest that acute Hyperglycemia may induce VED by decreasing NO bioavailability through an oxidative stress-dependent mechanism. Additional work is warranted to define whether inhibiting lipid peroxidation and restoring arginine metabolism would mitigate Hyperglycemia-mediated decreases in vascular function.
Gang Peng - One of the best experts on this subject based on the ideXlab platform.
-
Punica granatum flower extract, a potent α-glucosidase inhibitor, improves Postprandial Hyperglycemia in Zucker diabetic fatty rats
Journal of ethnopharmacology, 2005Co-Authors: Suping Wen, Gang Peng, Johji Yamahara, Bhavani Prasad Kota, Basil D. RoufogalisAbstract:Postprandial Hyperglycemia plays an important role in the development of type 2 diabetes and has been proposed as an independent risk factor for cardiovascular diseases. The flowering part of Punica granatum Linn. (Punicaceae) (PGF) has been recommended in Unani literature as a remedy for diabetes. We investigated the effect and action mechanism of a methanolic extract from PGF on Hyperglycemia in vivo and in vitro. Oral administration of PGF extract markedly lowered plasma glucose levels in non-fasted Zucker diabetic fatty rats (a genetic model of obesity and type 2 diabetes), whereas it had little effect in the fasted animals, suggesting it affected Postprandial Hyperglycemia in type 2 diabetes. In support of this conclusion the extract was found to markedly inhibit the increase of plasma glucose levels after sucrose loading, but not after glucose loading in mice, and it had no effect on glucose levels in normal mice. In vitro, PGF extract demonstrated a potent inhibitory effect on alpha-glucosidase activity (IC50: 1.8 microg/ml). The inhibition is dependent on the concentration of enzyme and substrate, as well as on the length of pretreatment with the enzyme. These findings strongly suggest that PGF extract improves Postprandial Hyperglycemia in type 2 diabetes and obesity, at least in part, by inhibiting intestinal alpha-glucosidase activity.
-
Salacia oblonga improves cardiac fibrosis and inhibits Postprandial Hyperglycemia in obese Zucker rats.
Life sciences, 2004Co-Authors: Gang Peng, Li Qian, Suping Wen, Tom Hsun-wei Huang, Basil D. Roufogalis, Johji YamaharaAbstract:Diabetes has a markedly greater incidence of cardiovascular disease than the non-diabetic population. The heart shows a slowly developing increase in fibrosis in diabetes. Extended cardiac fibrosis results in increased myocardial stiffness, causing ventricular dysfunction and, ultimately, heart failure. Reversal of fibrosis may improve organ function survival. Postprandial Hyperglycemia plays an important role in the development of type 2 diabetes and cardiovascular complications, and has been proposed as an independent risk factor for cardiovascular diseases. Salacia oblonga (S.O.) is traditionally used in the prevention and treatment of diabetes. We investigated the effects of its water extract on cardiac fibrosis and Hyperglycemia in a genetic model of type 2 diabetes, the obese Zucker rat (OZR). Chronic administration of the extract markedly improved interstitial and perivascular fibrosis in the hearts of the OZR. It also reduced plasma glucose levels in non-fasted OZR, whereas it had little effect in the fasted animals, suggesting inhibition of Postprandial Hyperglycemia in type 2 diabetic animals, which might play a role in improvement of the cardiac complications of OZR. Furthermore, S.O. markedly suppressed the overexpression of mRNAs encoding transforming growth factor betas 1 and 3 in the OZR heart, which may be an important part of the overall molecular mechanisms. S.O. dose-dependently inhibited the increase of plasma glucose in sucrose-, but not in glucose-loaded mice. S.O. demonstrated a strong inhibition of alpha-glucosidase activity in vitro, which is suggested to contribute to the improvement of Postprandial Hyperglycemia.
-
salacia oblonga improves cardiac fibrosis and inhibits Postprandial Hyperglycemia in obese zucker rats
Life Sciences, 2004Co-Authors: Gang Peng, Suping Wen, Tom Hsun-wei Huang, Basil D. Roufogalis, Johji YamaharaAbstract:Diabetes has a markedly greater incidence of cardiovascular disease than the non-diabetic population. The heart shows a slowly developing increase in fibrosis in diabetes. Extended cardiac fibrosis results in increased myocardial stiffness, causing ventricular dysfunction and, ultimately, heart failure. Reversal of fibrosis may improve organ function survival. Postprandial Hyperglycemia plays an important role in the development of type 2 diabetes and cardiovascular complications, and has been proposed as an independent risk factor for cardiovascular diseases. Salacia oblonga (S.O.) is traditionally used in the prevention and treatment of diabetes. We investigated the effects of its water extract on cardiac fibrosis and Hyperglycemia in a genetic model of type 2 diabetes, the obese Zucker rat (OZR). Chronic administration of the extract markedly improved interstitial and perivascular fibrosis in the hearts of the OZR. It also reduced plasma glucose levels in non-fasted OZR, whereas it had little effect in the fasted animals, suggesting inhibition of Postprandial Hyperglycemia in type 2 diabetic animals, which might play a role in improvement of the cardiac complications of OZR. Furthermore, S.O. markedly suppressed the overexpression of mRNAs encoding transforming growth factor βs 1 and 3 in the OZR heart, which may be an important part of the overall molecular mechanisms. S.O. dose-dependently inhibited the increase of plasma glucose in sucrose-, but not in glucose-loaded mice. S.O. demonstrated a strong inhibition of α-glucosidase activity in vitro, which is suggested to contribute to the improvement of Postprandial Hyperglycemia.
Levimar R. Araújo - One of the best experts on this subject based on the ideXlab platform.
-
efficacy of continuous glucose monitoring system cgms to detect Postprandial Hyperglycemia and unrecognized hypoglycemia in type 1 diabetic patients
Diabetes Research and Clinical Practice, 2007Co-Authors: Frederico F.r. Maia, Levimar R. AraújoAbstract:Abstract Background To evaluate the efficacy of continuous glucose monitoring system (CGMS) to detect Postprandial Hyperglycemia and unrecognized hypoglycemia in type 1 diabetes mellitus (DM1) patients. Methods We studied 46 patients (43.4%M/56.6%F), average age of 25.9±12.8 years, submitted to 72h CGMS. It were analyzed: capillary glycemia (CG) and CGMS sensor's value, glycemic excursions, Postprandial Hyperglycemia, asymptomatic hypoglycemia and therapeutic management after CGMS. Correlation coefficient during hypo and Hyperglycemia and sensitivity/specificity were determined. Results The mean capillary glucose values were 191.8±46.2mg/dl versus 190.9±42.1mg/dl by CGMS sensor, with no statistical difference by T -test ( T =−0.6; p =0.79). The CGMS was significantly more efficient in detection of glycemic excursion than CG ( p =0.001). The Postprandial Hyperglycemia was identified in 76.9% of diabetic patients and asymptomatic hypoglycemia was detected in 58.2% of these patients. The correlation coefficient presented no significance ( p =0.16) during hypoglycemia versus during Hyperglycemia ( p =0.002). The CGMS sensor presented low sensitivity (79.1%) to detect hypoglycemia versus Hyperglycemia (96.8%). Conclusions The CGMS showed to be a good method to identify Postprandial Hyperglycemia, to improve therapeutics management and confirmed the low sensitivity of CGMS to detect unrecognized hypoglycemia in DM1 patients.
-
Efficacy of continuous glucose monitoring system (CGMS) to detect Postprandial Hyperglycemia and unrecognized hypoglycemia in type 1 diabetic patients.
Diabetes research and clinical practice, 2006Co-Authors: Frederico F.r. Maia, Levimar R. AraújoAbstract:To evaluate the efficacy of continuous glucose monitoring system (CGMS) to detect Postprandial Hyperglycemia and unrecognized hypoglycemia in type 1 diabetes mellitus (DM1) patients. We studied 46 patients (43.4%M/56.6%F), average age of 25.9+/-12.8 years, submitted to 72 h CGMS. It were analyzed: capillary glycemia (CG) and CGMS sensor's value, glycemic excursions, Postprandial Hyperglycemia, asymptomatic hypoglycemia and therapeutic management after CGMS. Correlation coefficient during hypo and Hyperglycemia and sensitivity/specificity were determined. The mean capillary glucose values were 191.8+/-46.2mg/dl versus 190.9+/-42.1mg/dl by CGMS sensor, with no statistical difference by T-test (T=-0.6; p=0.79). The CGMS was significantly more efficient in detection of glycemic excursion than CG (p=0.001). The Postprandial Hyperglycemia was identified in 76.9% of diabetic patients and asymptomatic hypoglycemia was detected in 58.2% of these patients. The correlation coefficient presented no significance (p=0.16) during hypoglycemia versus during Hyperglycemia (p=0.002). The CGMS sensor presented low sensitivity (79.1%) to detect hypoglycemia versus Hyperglycemia (96.8%). The CGMS showed to be a good method to identify Postprandial Hyperglycemia, to improve therapeutics management and confirmed the low sensitivity of CGMS to detect unrecognized hypoglycemia in DM1 patients.