scholarly journals Abdominal Obesity, Insulin Resistance, and Very Low-Density Lipoprotein Subclass Profile in Japanese School Children

2016 ◽  
Vol 01 (01) ◽  
Author(s):  
Yuriko Abe ◽  
Tomoo Okada ◽  
Hiromi Okuma ◽  
Minako Kazama ◽  
Ryuta Yonezawa ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Abdominal Obesity ◽  
School Children ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Subclass

scholarly journals Mechanisms of Hepatic Very Low Density Lipoprotein Overproduction in Insulin Resistance

2000 ◽  
Vol 275 (12) ◽  
pp. 8416-8425 ◽  
Author(s):  
Changiz Taghibiglou ◽  
André Carpentier ◽  
Stephen C. Van Iderstine ◽  
Biao Chen ◽  
Debbie Rudy ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

Mechanisms of Hepatic Very Low-Density Lipoprotein Overproduction in Insulin Resistance

2001 ◽  
Vol 11 (5) ◽  
pp. 170-176 ◽  
Author(s):  
Khosrow Adeli ◽  
Changiz Taghibiglou ◽  
Stephen C Van Iderstine ◽  
Gary F Lewis
Keyword(s):  
Insulin Resistance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

scholarly journals Is There a Relation Between Triglyceride Concentrations in Very Low Density Lipoprotein and the Index of Insulin Resistance in Nondiabetic Subjects?

2014 ◽  
Vol 28 (4) ◽  
pp. 269-274 ◽  
Author(s):  
Yoshifumi Kurosaki ◽  
Tomoaki Tsukushi ◽  
Shinichi Munekata ◽  
Yuhsaku Kanoh ◽  
Tatsumi Moriya ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

scholarly journals Very Low Density Lipoprotein Metabolism and Plasma Adiponectin as Predictors of High-Density Lipoprotein Apolipoprotein A-I Kinetics in Obese and Nonobese Men

2009 ◽  
Vol 94 (3) ◽  
pp. 989-997 ◽  
Author(s):  
Dick C. Chan ◽  
P. Hugh R. Barrett ◽  
Esther M. M. Ooi ◽  
Juying Ji ◽  
Doris T. Chan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Density Lipoprotein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Plasma Adiponectin ◽  
Amyloid A ◽  
Vldl Metabolism

Abstract Context: Hypercatabolism of high-density lipoprotein (HDL) apolipoprotein (apo) A-I results in low plasma apoA-I concentration. The mechanisms regulating apoA-I catabolism may relate to alterations in very low density lipoprotein (VLDL) metabolism and plasma adiponectin and serum amyloid A protein (SAA) concentrations. Objective: We examined the associations between the fractional catabolic rate (FCR) of HDL-apoA-I and VLDL kinetics, plasma adiponectin, and SAA concentrations. Study Design: The kinetics of HDL-apoA-I and VLDL-apoB were measured in 50 obese and 37 nonobese men using stable isotopic techniques. Results: In the obese group, HDL-apoA-I FCR was positively correlated with insulin, homeostasis model of assessment for insulin resistance (HOMA-IR) score, triglycerides, VLDL-apoB, and VLDL-apoB production rate (PR). In the nonobese group, HDL-apoA-I FCR was positively correlated with triglycerides, apoC-III, VLDL-apoB, and VLDL-apoB PR and negatively correlated with plasma adiponectin. Plasma SAA was not associated with HDL-apoA-I FCR in either group. In multiple regression analyses, VLDL-apoB PR and HOMA-IR score, and VLDL-apoB PR and adiponectin were independently predictive of HDL-apoA-I FCR in the obese and nonobese groups, respectively. HDL-apoA-I FCR was positively and strongly associated with HDL-apoA-I PR in both groups. Conclusions: Variation in VLDL-apoB production, and hence plasma triglyceride concentrations, exerts a major effect on the catabolism of HDL-apoA-I. Insulin resistance and adiponectin may also contribute to the variation in HDL-apoA-I catabolism in obese and nonobese subjects, respectively. We also hypothesize that apoA-I PR determines a steady-state, lowered plasma of apoA-I, which may reflect a compensatory response to a primary defect in the catabolism of HDL-apoA-I due to altered VLDL metabolism.

scholarly journals Low-dose dexamethasone administration for 3 weeks favorably affects plasma HDL concentration and composition but does not affect very low-density lipoprotein kinetics

2012 ◽  
Vol 167 (2) ◽  
pp. 217-223 ◽  
Author(s):  
Xuewen Wang ◽  
Faidon Magkos ◽  
Bruce W Patterson ◽  
Dominic N Reeds ◽  
Janine Kampelman ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Plasma Lipoprotein ◽  
Metabolic Effects ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Particle Sizes ◽  
Lipoprotein Subclass ◽  
The Metabolic Syndrome

ObjectiveSubclinical hypercortisolemia often occurs in subjects with features of the metabolic syndrome, and it has been suggested that it may be, at least in part, responsible for the development of these metabolic abnormalities. However, the metabolic effects of glucocorticoid administration to mimic subclinical glucocorticoid excess have not been evaluated.MethodsWe used stable isotope-labeled tracer methods in conjunction with magnetic resonance techniques to measure the effect of glucocorticoid excess within the physiological range (∼0.7 mg dexamethasone/day for 3 weeks) on glucose and free fatty acid (FFA) rates of appearance (Ra) into plasma, intrahepatic triglyceride (TG) content, very low-density lipoprotein (VLDL)-TG and VLDL-apolipoprotein B-100 (apoB-100) kinetics and plasma lipoprotein subclass concentrations, and particle sizes in nine overweight and obese individuals.ResultsDexamethasone treatment led to a very small but significant increase in body weight (from 87.4±7.1 to 88.6±7.2 kg; P=0.003) and increased HDL-cholesterol (from 45.9±2.8 to 55.1±4.6 mg/dl; P=0.037) and HDL particle (from 33.7±2.2 to 41.4±4.2 nmol/l; P=0.023) concentrations in plasma but had no effect on intrahepatic TG content, glucose and FFA Ra in plasma, hepatic VLDL-TG and VLDL-apoB-100 secretion rates and mean residence times in the circulation, plasma TG and LDL-cholesterol concentrations, and plasma lipoprotein particle sizes.ConclusionSubclinical hypercortisolemia does not have significant adverse metabolic consequences.

scholarly journals Dyslipidemia is the hallmark of the metabolic syndrome in postmenopausal women

2020 ◽  
Vol 4 (2) ◽  
pp. 18-21
Author(s):  
Asim Alaaeldin Osman ◽  
Ahmed Mohamed Fadlalla
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Total Cholesterol ◽  
Postmenopausal Women ◽  
Lipid Accumulation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Significant Negative Correlation ◽  
Very Low Density Lipoprotein ◽  
Low Density

The incidence of cardiovascular diseases (CVD) increases after menopause and may be due to changes in the plasma lipid-lipoprotein levels that occur following menopausal transition. Physiological estrogen withdrawal during menopause plays a major role in abnormal lipid metabolism such as elevated low-density lipoprotein concentration. The aim of this study was to determine the relationship between dyslipidemia and the causative factors of metabolic syndrome in postmenopausal women. In this cross-sectional study, 290 postmenopausal Sudanese women were included. Lipid profiles were measured by spectrophotometer, estrogen hormone determined by ELISA, insulin resistance determined by HOMA-2 calculator and lipid accumulation product was calculated by the following equation (waist circumference in cm X triglyceride concentration in mM). The results revealed that total cholesterol, triglycerides, low-density lipoprotein levels and very low-density lipoprotein levels were significantly higher in the postmenopausal women with metabolic syndrome (MS) in comparison to those without the MS. Elevated total cholesterol levels were seen in 51.7 %, elevated triglycerides were seen in 49.7% and elevated low-density lipoprotein levels were seen in 29.3% whereas reduced high density lipoprotein levels were seen in 16.89% of the postmenopausal women. Total cholesterol, triglycerides and very low-density lipoprotein values showed a significant positive correlation with insulin resistance and lipid accumulation and a significant negative correlation with the estrogen hormone level. In addition, high density lipoproteins showed a significant negative correlation with lipid accumulation levels.

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