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hypertriglyceridemia
فَرْطُ ثُلاثِيِّ غليسيريدِ الدَّم
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alimentary hypertriglyceridemia
فَرْطُ ثُلاثِيِّ غليسيريدِ الدَّمِ الهَضْمِيُّ المَنْشَأ في الدَّم
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carbohydrate induced hypertriglyceridemia
فَرْطُ ثُلاثِيِّ غليسيريدِ الدَّمِ المُحَرَّضُ بالكَرْبُوهيدرات
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carbohydrate-induced hypertriglyceridemia
فَرْطُ ثُلاثِيِّ غليسيريدِ الدَّمِ المُحَرَّضُ بالكَرْبُوهيدرات
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intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity elisa fabbrini, faidon magkos, [...], and samuel klein additional article information associated data supplementary materials abstract visceral adipose tissue (vat) is an important risk factor for obesity-related metabolic disorders. therefore, a reduction in vat has become a key goal in obesity management. however, vat is correlated with intrahepatic triglyceride (ihtg) content, so it is possible that ihtg, not vat, is a better marker of metabolic disease. we determined the independent association of ihtg and vat to metabolic function, by evaluating groups of obese subjects, who differed in ihtg content (high or normal) but matched on vat volume or differed in vat volume (high or low) but matched on ihtg content. stable isotope tracer techniques and the euglycemic–hyperinsulinemic clamp procedure were used to assess insulin sensitivity and very-low-density lipoprotein–triglyceride (vldl-tg) secretion rate. tissue biopsies were obtained to evaluate cellular factors involved in ectopic triglyceride accumulation. hepatic, adipose tissue and muscle insulin sensitivity were 41, 13, and 36% lower (p < 0.01), whereas vldl-triglyceride secretion rate was almost double (p < 0.001), in subjects with higher than normal ihtg content, matched on vat. no differences in insulin sensitivity or vldl-tg secretion were observed between subjects with different vat volumes, matched on ihtg content. adipose tissue cd36 expression was lower (p < 0.05), whereas skeletal muscle cd36 expression was higher (p < 0.05), in subjects with higher than normal ihtg. these data demonstrate that ihtg, not vat, is a better marker of the metabolic derangements associated with obesity. furthermore, alterations in tissue fatty acid transport could be involved in the pathogenesis of ectopic triglyceride accumulation by redirecting plasma fatty acid uptake from adipose tissue toward other tissues. keywords: abdominal fat, insulin resistance, nafld, steatosis, vldl visceral adipose tissue (vat) is an important and independent predictor of metabolic risk factors for coronary heart disease, particularly diabetes and dyslipidemia (1, 2). moreover, data from metabolic studies conducted on human subjects (3, 4) indicate that an increase in vat is associated with impaired glucose tolerance, insulin resistance, and increased very-low-density lipoprotein–triglyceride (vldl-tg) secretion. these observations and the unique anatomical location of visceral fat, which releases free fatty acids (ffa) and adipokines into the portal vein for direct transport to the liver, have led to the concept that vat is responsible for many of the metabolic abnormalities associated with abdominal obesity (5, 6). therefore, a reduction in visceral fat has become a key therapeutic goal in the management of obesity (6, 7). although vat is associated with metabolic disease, a causal link between vat and metabolic dysfunction has not been demonstrated in humans. recently, it has become clear that vat correlates directly with intrahepatic triglyceride (ihtg) content (8–10), and an increase in ihtg is associated with the same metabolic abnormalities linked to an increase in vat (9–12). therefore, it is possible that vat itself is not harmful, but is simply an innocent bystander that tracks with ihtg. the mechanism(s) responsible for the interrelationship among ihtg content, insulin resistance, and hypertriglyceridemia is not known, but could involve redirecting plasma ffa uptake and intracellular triglyceride production from adipose tissue depots to other tissues, such as liver and skeletal muscle, which can impair insulin signaling (13, 14) and stimulate vldl-tg secretion (11). therefore, it is possible that organ-specific alterations in cd36, which regulates tissue ffa uptake from plasma (15), are involved in the pathogenesis of ectopic triglyceride accumulation and metabolic disease. the purpose of the present study was to test the hypotheses that (i) high ihtg content, not increased vat volume, is the primary marker of metabolic abnormalities associated with obesity and (ii) high ihtg content is associated with alterations in adipose tissue and skeletal muscle cd36 gene expression and protein content that are consistent with redirecting plasma fatty acids away from adipose tissue and toward other metabolic organs. both in vivo and cellular metabolic assessments were conducted in obese subjects, who were carefully matched on either ihtg content or vat volume, to help separate the potential influence of ihtg and vat on metabolic function. stable isotope tracer infusions in conjunction with mathematical modeling were used to evaluate hepatic, skeletal muscle and adipose tissue insulin sensitivity, and vldl-tg secretion rate, while adipose tissue and skeletal muscle biopsies were used to determine cellular cd36 gene expression and protein content. results body composition. subjects in each group were matched on age, sex, body mass index (bmi), and percentage of body fat, but differed in either ihtg content or vat volume (table 1). mean ihtg content in the high-ihtg groups was 5-fold greater than in the normal-ihtg groups, and mean vat volume in the high-vat group was 2-fold greater than in the low-vat group (table 1). table 1. table 1. subject characteristics in each study group plasma metabolic variables. plasma insulin concentration was almost 2-fold greater and plasma adiponectin concentration was ≈50% lower in subjects with high ihtg content than in those with normal ihtg who were matched on vat volume (table 2). no significant differences in metabolic variables were detected between subjects with low or high vat volume who were matched on ihtg content (table 2).
Last Update: 2021-04-14
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