scholarly journals Cinnamon increases liver glycogen, improves insulin sensitivity, and regulates glycogen synthesis related gene expression in an animal model of the metabolic syndrome

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Bolin Qin ◽  
Karine Couturier ◽  
Cecile Batandier ◽  
Manar Awada ◽  
Isabelle Hininger‐Favier ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Animal Model ◽  
Insulin Sensitivity ◽  
Glycogen Synthesis ◽  
Liver Glycogen ◽  
Related Gene ◽  
The Metabolic Syndrome

scholarly journals Adiponectin Gene Expression and Plasma Values in Obese Women during Very-Low-Calorie Diet. Relationship with Cardiovascular Risk Factors and Insulin Resistance

2004 ◽  
Vol 89 (2) ◽  
pp. 756-760 ◽  
Author(s):  
Marta Garaulet ◽  
Nathalie Viguerie ◽  
Stefan Porubsky ◽  
Eva Klimcakova ◽  
Karine Clement ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Obese Women ◽  
Adiponectin Gene ◽  
Very Low Calorie Diet ◽  
Plasma Adiponectin ◽  
The Metabolic Syndrome ◽  
Low Calorie Diet ◽  
Calorie Diet

Adiponectin, a newly discovered adipose-tissue-specific protein, is thought to be involved in the regulation of insulin action. The aim of the present study was to determine whether adiponectin contributes to the improvement in insulin sensitivity during very-low-calorie diet (VLCD). Biopsies of sc abdominal adipose tissue and blood sampling for analysis of plasma adiponectin and related hormones and metabolites were performed before and at the end of a 4-wk VLCD in 33 nonmorbidly obese women (body mass index, 34.4 ± 4.1 kg/m2). VLCD produced a decrease in weight (7.1 ± 0.4 kg) and in insulin and leptin levels and led to an improvement in insulin sensitivity. Adiponectin gene expression and plasma levels were not modified during calorie restriction. Before VLCD, we found negative correlations between plasma adiponectin and variables related to the metabolic syndrome. Adiponectin mRNA levels showed a negative correlation with lipoprotein a plasma values. The correlations observed before VLCD were not found after VLCD. The data suggest that adiponectin is related to the protection against the metabolic syndrome but is not involved in the regulation of VLCD-induced improvement of insulin sensitivity.

Cinnamon improves insulin sensitivity and alters the body composition in an animal model of the metabolic syndrome

2010 ◽  
Vol 501 (1) ◽  
pp. 158-161 ◽  
Author(s):  
K. Couturier ◽  
C. Batandier ◽  
M. Awada ◽  
I. Hininger-Favier ◽  
F. Canini ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Animal Model ◽  
Body Composition ◽  
Insulin Sensitivity ◽  
The Body ◽  
The Metabolic Syndrome

scholarly journals Global metabolic consequences of the chromogranin A-null model of hypertension: transcriptomic detection, pathway identification, and experimental verification

2010 ◽  
Vol 40 (3) ◽  
pp. 195-207 ◽  
Author(s):  
Ryan S. Friese ◽  
Jiaur R. Gayen ◽  
Nitish R. Mahapatra ◽  
Geert W. Schmid-Schönbein ◽  
Daniel T. O'Connor ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Chromogranin A ◽  
Secretory Granules ◽  
Cholesterol Biosynthesis ◽  
Hepatic Cholesterol ◽  
The Metabolic Syndrome ◽  
Insight Into

Chromogranin A (CHGA) has a crucial role in formation of regulated secretory granules in neuroendocrine tissues and is also a prohormone that is proteolytically processed into peptides with diverse and complex actions. CHGA and several of its peptide products, including catestatin and pancreastatin, are implicated in pathogenesis of essential hypertension, insulin resistance, and the metabolic syndrome. The Chga knockout mouse (Chga KO) displays severe hypertension coupled with reduction in size, number, and density of regulated secretory granules. We performed genome-wide transcriptome profiling in Chga KO adrenal gland and liver for insight into biochemical and physiological systems altered in this monogenic mouse model of hypertension. Adrenal gene expression pathway prediction of enhanced insulin sensitivity ( P = 0.03) in Chga KO was confirmed with glucose, insulin, and homeostasis model assessment of insulin resistance (HOMA-IR) measurements: blood glucose was normal in Chga KO, blood insulin was reduced 4.5-fold ( P < 0.0001), and HOMA-IR was decreased 3.8-fold ( P < 0.002). Remarkably, such observations conclusively dissociate fundamental features of the metabolic syndrome in this monogenic hypertension model. Exogenous pancreastatin treatment restored insulin sensitivity in the Chga KO to near-normal levels. Gene expression predictions of decreased adrenal cholesterol biosynthesis ( P < 0.001) and increased hepatic cholesterol biosynthesis ( P < 0.001) were verified with tissue total cholesterol assays: Chga KO adrenal cholesterol decreased 1.8-fold ( P = 0.039) and hepatic cholesterol increased 1.8-fold ( P = 0.018). Transcriptional regulatory network prediction identified sets of transcription factors that may provide insight into the unclear mechanistic links among CHGA, cholesterol, insulin sensitivity, and the metabolic syndrome. These experiments demonstrate, for the first time, that genetic variation at the CHGA locus impacts insulin sensitivity and tissue cholesterol levels in an intact, living organism. The Chga KO may constitute a unique model for studying the relationship between the CHGA locus and disease phenotypes of the metabolic syndrome.

Effect of Colesevelam Hydrochloride on Glycemia and Insulin Sensitivity in Men With the Metabolic Syndrome

2011 ◽  
Vol 108 (8) ◽  
pp. 1129-1135 ◽  
Author(s):  
Gloria Lena Vega ◽  
Fredrick L. Dunn ◽  
Scott M. Grundy
Keyword(s):  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
The Metabolic Syndrome

Integrating Genetic and Gene Expression Data to Study the Metabolic Syndrome and Diabetes in Mice

2005 ◽  
Vol 12 (6) ◽  
pp. 503-511 ◽  
Author(s):  
Thomas A Drake ◽  
Eric E Schadt ◽  
Richard C Davis ◽  
Aldons J Lusis
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Gene Expression Data ◽  
Expression Data ◽  
The Metabolic Syndrome ◽  
Diabetes In Mice

scholarly journals The Metabolic Syndrome in Overweight Hispanic Youth and the Role of Insulin Sensitivity

2004 ◽  
Vol 89 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Martha L. Cruz ◽  
Marc J. Weigensberg ◽  
Terry T.-K. Huang ◽  
Geoff Ball ◽  
Gabriel Q. Shaibi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Family History ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Hdl Cholesterol ◽  
Hispanic Youth ◽  
The Metabolic Syndrome

The prevalence of the metabolic syndrome is highest among Hispanic adults. However, studies exploring the metabolic syndrome in overweight Hispanic youth are lacking. Subjects were 126 overweight children (8–13 yr of age) with a family history for type 2 diabetes. The metabolic syndrome was defined as having at least three of the following: abdominal obesity, low high-density lipoprotein (HDL) cholesterol, hypertriglyceridemia, hypertension, and/or impaired glucose tolerance. Insulin sensitivity was determined by the frequently sampled iv glucose tolerance test and minimal modeling. The prevalence of abdominal obesity, low HDL cholesterol, hypertriglyceridemia, systolic and diastolic hypertension, and impaired glucose tolerance was 62, 67, 26, 22, 4, and 27%, respectively. The presence of zero, one, two, or three or more features of the metabolic syndrome was 9, 22, 38, and 30%, respectively. After controlling for body composition, insulin sensitivity was positively related to HDL cholesterol (P &lt; 0.01) and negatively related to triglycerides (P &lt; 0.001) and systolic (P &lt; 0.01) and diastolic blood pressure (P &lt; 0.05). Insulin sensitivity significantly decreased (P &lt; 0.001) as the number of features of the metabolic syndrome increased. In conclusion, overweight Hispanic youth with a family history for type 2 diabetes are at increased risk for cardiovascular disease and type 2 diabetes, and this appears to be due to decreased insulin sensitivity. Improving insulin resistance may be crucial for the prevention of chronic disease in this at-risk population.

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