The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
Kui Li - One of the best experts on this subject based on the ideXlab platform.
-
Global Transcriptomic Profiling of Cardiac Hypertrophy and Fatty Heart Induced by Long-Term High-Energy Diet in Bama Miniature Pigs.
PLOS ONE, 2015Co-Authors: Yuanyuan Zhang, Siyuan Kong, Yaoxing Chen, Shulin Yang, Kui LiAbstract:A long-term High-Energy Diet affects human health and leads to obesity and metabolic syndrome in addition to cardiac steatosis and hypertrophy. Ectopic fat accumulation in the heart has been demonstrated to be a risk factor for heart disorders, but the molecular mechanism of heart disease remains largely unknown. Bama miniature pigs were fed a High-fat, High-sucrose Diet (HFHSD) for 23 months. These pigs developed symptoms of metabolic syndrome and showed cardiac steatosis and hypertrophy with a greatly increased body weight (2.73-fold, P
-
global transcriptomic profiling of cardiac hypertrophy and fatty heart induced by long term High Energy Diet in bama miniature pigs
PLOS ONE, 2015Co-Authors: Yuanyuan Zhang, Siyuan Kong, Yaoxing Chen, Shulin Yang, Kui LiAbstract:A long-term High-Energy Diet affects human health and leads to obesity and metabolic syndrome in addition to cardiac steatosis and hypertrophy. Ectopic fat accumulation in the heart has been demonstrated to be a risk factor for heart disorders, but the molecular mechanism of heart disease remains largely unknown. Bama miniature pigs were fed a High-fat, High-sucrose Diet (HFHSD) for 23 months. These pigs developed symptoms of metabolic syndrome and showed cardiac steatosis and hypertrophy with a greatly increased body weight (2.73-fold, P<0.01), insulin level (4.60-fold, P<0.01), heart weight (1.82-fold, P<0.05) and heart volume (1.60-fold, P<0.05) compared with the control pigs. To understand the molecular mechanisms of cardiac steatosis and hypertrophy, nine pig heart cRNA samples were hybridized to porcine GeneChips. Microarray analyses revealed that 1,022 genes were significantly differentially expressed (P<0.05, ≥1.5-fold change), including 591 up-regulated and 431 down-regulated genes in the HFHSD group relative to the control group. KEGG analysis indicated that the observed heart disorder involved the signal transduction-related MAPK, cytokine, and PPAR signaling pathways, Energy metabolism-related fatty acid and oxidative phosphorylation signaling pathways, heart function signaling-related focal adhesion, axon guidance, hypertrophic cardiomyopathy and actin cytoskeleton signaling pathways, inflammation and apoptosis pathways, and others. Quantitative RT-PCR assays identified several important differentially expressed heart-related genes, including STAT3, ACSL4, ATF4, FADD, PPP3CA, CD74, SLA-8, VCL, ACTN2 and FGFR1, which may be targets of further research. This study shows that a long-term, High-Energy Diet induces obesity, cardiac steatosis, and hypertrophy and provides insights into the molecular mechanisms of hypertrophy and fatty heart to facilitate further research.
Forrest H Nielsen - One of the best experts on this subject based on the ideXlab platform.
-
Dietary boron does not affect tooth strength, micro-hardness, and density, but affects tooth mineral composition and alveolar bone mineral density in rabbits fed a High-Energy Diet
Journal of Trace Elements in Medicine and Biology, 2014Co-Authors: Sema S Hakki, Niyazi Dundar, Seyit Ali Kayis, Erdogan E Hakki, Mehmet Hamurcu, Nuri Baspinar, Abdullah Basoglu, Forrest H Nielsen, Sıddık Malkoç, Werner GötzAbstract:Abstract The objective of this study was to determine whether Dietary boron (B) affects the strength, density and mineral composition of teeth and mineral density of alveolar bone in rabbits with apparent obesity induced by a High-Energy Diet. Sixty female, 8-month-old, New Zealand rabbits were randomly assigned for 7 months into five groups as follows: (1) control 1, fed alfalfa hay only (5.91 MJ/kg and 57.5 mg B/kg); (2) control 2, High Energy Diet (11.76 MJ and 3.88 mg B/kg); (3) B10, High Energy Diet + 10 mg B gavage/kg body weight/96 h; (4) B30, High Energy Diet + 30 mg B gavage/kg body weight/96 h; (5) B50, High Energy Diet + 50 mg B gavage/kg body weight/96 h. Maxillary incisor teeth of the rabbits were evaluated for compression strength, mineral composition, and micro-hardness. Enamel, dentin, cementum and pulp tissue were examined histologically. Mineral densities of the incisor teeth and surrounding alveolar bone were determined by using micro-CT. When compared to controls, the different boron treatments did not significantly affect compression strength, and micro-hardness of the teeth, although the B content of teeth increased in a dose-dependent manner. Compared to control 1, B50 teeth had decreased phosphorus (P) concentrations. Histological examination revealed that teeth structure (shape and thickness of the enamel, dentin, cementum and pulp) was similar in the B-treated and control rabbits. Micro CT evaluation revealed greater alveolar bone mineral density in B10 and B30 groups than in controls. Alveolar bone density of the B50 group was not different than the controls. Although the B treatments did not affect teeth structure, strength, mineral density and micro-hardness, increasing B intake altered the mineral composition of teeth, and, in moderate amounts, had beneficial effects on surrounding alveolar bone.
-
boron enhances strength and alters mineral composition of bone in rabbits fed a High Energy Diet
Journal of Trace Elements in Medicine and Biology, 2013Co-Authors: Sema S Hakki, Niyazi Dundar, Seyit Ali Kayis, Erdogan E Hakki, Mehmet Hamurcu, Ulku Kerimoglu, Nuri Baspinar, Abdullah Basoglu, Forrest H NielsenAbstract:Summary An experiment was performed to determine whether boron had a beneficial effect on bone strength and composition in rabbits with apparent adiposity induced by a High Energy Diet. Sixty female New Zealand rabbits, aged 8 months, were randomly divided into five groups with the following treatments for seven months: control 1, fed alfalfa hay only (5.91 MJ/kg); control 2, High Energy Diet (11.76 MJ and 3.88 mg boron/kg); B10, High Energy Diet + 10 mg/kg body weight boron gavage/96 h; B30, High Energy Diet + 30 mg/kg body weight boron gavage/96 h; B50, High Energy Diet + 50 mg/kg body weight boron gavage/96 h. Bone boron concentrations were lowest in rabbits fed the High Energy Diet without boron supplementation, which suggested an inferior boron status. Femur maximum breaking force was Highest in the B50 rabbits. Tibia compression strength was Highest in B30 and B50 rabbits. All boron treatments significantly increased calcium and magnesium concentrations, and the B30 and B50 treatments increased the phosphorus concentration in tibia of rabbits fed the High Energy Diet. The B30 treatment significantly increased calcium, phosphorus and magnesium concentrations in femur of rabbits fed the High Energy Diet. Principal component analysis of the tibia minerals showed that the three boron treatments formed a separate cluster from controls. Discriminant analysis suggested that the concentrations of the minerals in femur could predict boron treatment. The findings indicate boron has beneficial effects on bone strength and mineral composition in rabbits fed a High Energy Diet.
Michael Pollak - One of the best experts on this subject based on the ideXlab platform.
-
metformin blocks the stimulative effect of a High Energy Diet on colon carcinoma growth in vivo and is associated with reduced expression of fatty acid synthase
Endocrine-related Cancer, 2010Co-Authors: Carolyn Algire, Mahvash Zakikhani, Lilian Amrein, Lawrence Panasci, Michael PollakAbstract:The molecular mechanisms responsible for the association of obesity with adverse colon cancer outcomes are poorly understood. We investigated the effects of a High-Energy Diet on growth of an in vivo colon cancer model. Seventeen days following the injection of 5!10 5 MC38 colon carcinoma cells, tumors from mice on the High-Energy Diet were approximately twice the volume of those of mice on the control Diet. These findings were correlated with the observation that the HighEnergy Diet led to elevated insulin levels, phosphorylated AKT, and increased expression of fatty acid synthase (FASN) by the tumor cells. Metformin, an antidiabetic drug, leads to the activation of AMPK and is currently under investigation for its antineoplastic activity. We observed that metformin blocked the effect of the High-Energy Diet on tumor growth, reduced insulin levels, and attenuated the effect of Diet on phosphorylation of AKT and expression of FASN. Furthermore, the administration of metformin led to the activation of AMPK, the inhibitory phosphorylation of acetyl-CoA carboxylase, the upregulation of BNIP3 and increased apoptosis as estimated by poly (ADP-ribose) polymerase (PARP) cleavage. Prior work showed that activating mutations of PI3K are associated with increased AKT activation and adverse outcome in colon cancer; our results demonstrate that the aggressive tumor behavior associated with a High-Energy Diet has similar effects on this signaling pathway. Furthermore, metformin is demonstrated to reverse the effects of the High-Energy Diet, thus suggesting a potential role for this agent in the management of a metabolically defined subset of colon cancers. Endocrine-Related Cancer (2010) 17 351–360
-
metformin attenuates the stimulatory effect of a High Energy Diet on in vivo llc1 carcinoma growth
Endocrine-related Cancer, 2008Co-Authors: Carolyn Algire, Mahvash Zakikhani, Mariejose Blouin, Jian Hua Shuai, Michael PollakAbstract:We investigated the effects of metformin on the growth of lewis lung LLC1 carcinoma in C57BL/6J mice provided with either a control Diet or a High-Energy Diet, previously reported to lead to weight gain and systemic insulin resistance with hyperinsulinemia. Forty-eight male mice were randomized into four groups: control Diet, control DietCmetformin, High-Energy Diet, or HighEnergy DietCmetformin. Following 8 weeks on the experimental Diets, selected groups received metformin in their drinking water. Three weeks following the start of metformin treatment, mice were injected with 0.5!10 6 LLC1 cells and tumor growth was measured for 17 days. By day 17, tumors of mice on the High-Energy Diet were nearly twice the volume of those of mice on the control Diet. This effect of Diet on tumor growth was significantly attenuated by metformin, but metformin had no effect on tumor growth of the mice on the control Diet. Metformin attenuated the increased insulin receptor activation associated with the High-Energy Diet and also led to increased phosphorylation of AMP kinase, two actions that would be expected to decrease neoplastic proliferation. These experimental results are consistent with prior hypothesisgenerating epidemiological studies that suggest that metformin may reduce cancer risk and improve cancer prognosis. Finally, these results contribute to the rationale for evaluation of the anti-neoplastic activity of metformin in hyperinsulinemic cancer patients. Endocrine-Related Cancer (2008) 15 833‐839
Carolyn Algire - One of the best experts on this subject based on the ideXlab platform.
-
metformin abolishes increased tumor 18f 2 fluoro 2 deoxy d glucose uptake associated with a High Energy Diet
Cell Cycle, 2011Co-Authors: Haider Mashhedi, Carolyn Algire, Mahvash Zakikhani, Mariejose Blouin, Stephanie David, Yunhua Zhao, Miguel Bazile, Elena Birman, Antonio Aliaga, Barry J BedellAbstract:Insulin regulates glucose uptake by normal tissues. Although there is evidence that certain cancers are growth-stimulated by insulin, the possibility that insulin influences tumor glucose uptake as assessed by 18F-2-Fluoro-2-Deoxy-d-Glucose Positron Emission Tomography (FDG-PET) has not been studied in detail. We present a model of Diet-induced hyperinsulinemia associated with increased insulin receptor activation in neoplastic tissue and with increased tumor FDG-PET image intensity. Metformin abolished the Diet-induced increases in serum insulin level, tumor insulin receptor activation and tumor FDG uptake associated with the High Energy Diet but had no effect on these measurements in mice on a control Diet. These findings provide the first functional imaging correlate of the well-known adverse effect of caloric excess on cancer outcome. They demonstrate that, for a subset of neoplasms, Diet and insulin are variables that affect tumor FDG uptake and have implications for design of clinical trials of metf...
-
metformin blocks the stimulative effect of a High Energy Diet on colon carcinoma growth in vivo and is associated with reduced expression of fatty acid synthase
Endocrine-related Cancer, 2010Co-Authors: Carolyn Algire, Mahvash Zakikhani, Lilian Amrein, Lawrence Panasci, Michael PollakAbstract:The molecular mechanisms responsible for the association of obesity with adverse colon cancer outcomes are poorly understood. We investigated the effects of a High-Energy Diet on growth of an in vivo colon cancer model. Seventeen days following the injection of 5!10 5 MC38 colon carcinoma cells, tumors from mice on the High-Energy Diet were approximately twice the volume of those of mice on the control Diet. These findings were correlated with the observation that the HighEnergy Diet led to elevated insulin levels, phosphorylated AKT, and increased expression of fatty acid synthase (FASN) by the tumor cells. Metformin, an antidiabetic drug, leads to the activation of AMPK and is currently under investigation for its antineoplastic activity. We observed that metformin blocked the effect of the High-Energy Diet on tumor growth, reduced insulin levels, and attenuated the effect of Diet on phosphorylation of AKT and expression of FASN. Furthermore, the administration of metformin led to the activation of AMPK, the inhibitory phosphorylation of acetyl-CoA carboxylase, the upregulation of BNIP3 and increased apoptosis as estimated by poly (ADP-ribose) polymerase (PARP) cleavage. Prior work showed that activating mutations of PI3K are associated with increased AKT activation and adverse outcome in colon cancer; our results demonstrate that the aggressive tumor behavior associated with a High-Energy Diet has similar effects on this signaling pathway. Furthermore, metformin is demonstrated to reverse the effects of the High-Energy Diet, thus suggesting a potential role for this agent in the management of a metabolically defined subset of colon cancers. Endocrine-Related Cancer (2010) 17 351–360
-
metformin attenuates the stimulatory effect of a High Energy Diet on in vivo llc1 carcinoma growth
Endocrine-related Cancer, 2008Co-Authors: Carolyn Algire, Mahvash Zakikhani, Mariejose Blouin, Jian Hua Shuai, Michael PollakAbstract:We investigated the effects of metformin on the growth of lewis lung LLC1 carcinoma in C57BL/6J mice provided with either a control Diet or a High-Energy Diet, previously reported to lead to weight gain and systemic insulin resistance with hyperinsulinemia. Forty-eight male mice were randomized into four groups: control Diet, control DietCmetformin, High-Energy Diet, or HighEnergy DietCmetformin. Following 8 weeks on the experimental Diets, selected groups received metformin in their drinking water. Three weeks following the start of metformin treatment, mice were injected with 0.5!10 6 LLC1 cells and tumor growth was measured for 17 days. By day 17, tumors of mice on the High-Energy Diet were nearly twice the volume of those of mice on the control Diet. This effect of Diet on tumor growth was significantly attenuated by metformin, but metformin had no effect on tumor growth of the mice on the control Diet. Metformin attenuated the increased insulin receptor activation associated with the High-Energy Diet and also led to increased phosphorylation of AMP kinase, two actions that would be expected to decrease neoplastic proliferation. These experimental results are consistent with prior hypothesisgenerating epidemiological studies that suggest that metformin may reduce cancer risk and improve cancer prognosis. Finally, these results contribute to the rationale for evaluation of the anti-neoplastic activity of metformin in hyperinsulinemic cancer patients. Endocrine-Related Cancer (2008) 15 833‐839
Barry J Bedell - One of the best experts on this subject based on the ideXlab platform.
-
metformin abolishes increased tumor 18f 2 fluoro 2 deoxy d glucose uptake associated with a High Energy Diet
Cell Cycle, 2011Co-Authors: Haider Mashhedi, Carolyn Algire, Mahvash Zakikhani, Mariejose Blouin, Stephanie David, Yunhua Zhao, Miguel Bazile, Elena Birman, Antonio Aliaga, Barry J BedellAbstract:Insulin regulates glucose uptake by normal tissues. Although there is evidence that certain cancers are growth-stimulated by insulin, the possibility that insulin influences tumor glucose uptake as assessed by 18F-2-Fluoro-2-Deoxy-d-Glucose Positron Emission Tomography (FDG-PET) has not been studied in detail. We present a model of Diet-induced hyperinsulinemia associated with increased insulin receptor activation in neoplastic tissue and with increased tumor FDG-PET image intensity. Metformin abolished the Diet-induced increases in serum insulin level, tumor insulin receptor activation and tumor FDG uptake associated with the High Energy Diet but had no effect on these measurements in mice on a control Diet. These findings provide the first functional imaging correlate of the well-known adverse effect of caloric excess on cancer outcome. They demonstrate that, for a subset of neoplasms, Diet and insulin are variables that affect tumor FDG uptake and have implications for design of clinical trials of metf...