Lipid mobilization in relation to body composition in man

Björntorp, Per; Bergman, Halvar; Varnauskas, E; Lindholm, B.

doi:10.1016/0026-0495(69)90059-6

Cited by 91 publications

(28 citation statements)

References 29 publications

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“…On the other hand, hGH treatment partially restored serum leptin levels without affecting serum insulin levels. In GHD adults, increased circulating leptin levels have previously been observed (22,23) and could be reduced by GH therapy. Under in vitro experimental conditions, GH does not affect leptin expression or secretion (24) and, therefore, it is likely that leptin levels in GHD adults reflect body composition rather than GH status.…”

Section: Discussionmentioning

confidence: 91%

Effects of pair-feeding and growth hormone treatment on obese transgenic rats

Furuhata

Hirabayashi²,

Yonezawa³

et al. 2002

European Journal of Endocrinology

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Background: It has been shown that GH-deficient subjects tend to have fat accumulation. We have produced human GH (hGH) transgenic rats that exhibit low circulating hGH levels and hyperphagia. These rats are also characterized by severe obesity, hyperinsulinemia and hyperlipidemia. Objective: The present study was conducted in order to elucidate how excess caloric intake and impaired GH secretion account for fat accumulation and metabolic abnormalities in the transgenic rats. Design and Methods: The transgenic rats were subjected to either pair-feeding with non-transgenic controls or hGH treatment from 4 to 12 weeks of age, and the effects on fat accumulation and some metabolic parameters were assessed. Results: At the age of 12 weeks, body weight and food intake were greater in transgenic than in control rats by 10% and 27% respectively. The ratio of epididymal white adipose tissue weight to body weight (WAT/BW) was more than three times greater in transgenic than in control rats. Although pair-feeding for 8 weeks decreased body weight, it did not affect the WAT/BW ratio. Treatment with hGH affected neither body weight nor food intake, while it reduced the WAT/BW ratio by 30%. Serum concentrations of triglyceride, free fatty acid, insulin and leptin were all significantly higher in the transgenic than in the control rats. Pair-feeding decreased serum triglyceride, insulin and leptin levels, but not serum free fatty acid levels. On the other hand, hGH treatment decreased only serum leptin concentrations. Conclusions: These results suggest that severe fat accumulation in the transgenic rats mainly resulted from the decreased lipolytic action of GH, while metabolic abnormalities mainly resulted from excess caloric intake.

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Section: Discussionmentioning

confidence: 91%

Effects of pair-feeding and growth hormone treatment on obese transgenic rats

Furuhata

Hirabayashi²,

Yonezawa³

et al. 2002

European Journal of Endocrinology

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“…One of the early indications of the defect in insulin secretion is selective impairment in GSIS. The great majority of type 2 diabetic individuals are obese and often have elevated plasma levels of FFA (Boden 1997), which seems to be a consequence of their expanded (Bjorntorp et al 1969) and more lipolytically active (Rebuffe-Scrive et al 1990) adipose tissue. It is well established that FFA can impair insulin action (Delarue & Magnan 2007) in peripheral tissues.…”

Section: Discussionmentioning

confidence: 99%

Ex vivo transcriptional profiling of human pancreatic islets following chronic exposure to monounsaturated fatty acids

Bikopoulos

Pimenta²,

Lee³

et al. 2007

Journal of Endocrinology

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The aim of this study was to assess the effects of chronic free fatty acid (FFA) exposure on gene expression and the functional state of human pancreatic islets. Chronic exposure of islets to oleate (OA) resulted in a significant reduction in glucose-stimulated insulin secretion (GSIS) compared with control (466G82 vs 234G57 ng/mg DNA, P!0 . 05). OA treatment also led to reduction in total insulin content of the islets (17 609G3816 vs 10 599G3876 ng insulin/mg DNA) and to an increase in the rate of reactive oxygen species (ROS) generation. Interestingly, the suppressive effects of OA on biosynthesis and secretion of insulin were accompanied by alteration in the expression of 40 genes, as determined by microarray analysis and subsequent qPCR validation. The majority of genes regulated by OA encoded metabolic enzymes. The expression of enzymes involved in oxidative defense was elevated, indicating a link between ROS generation and antioxidant defense activation. Additionally, pretreatment of human islets with OA led to a significant increase (30%) in the rate of oxidation of this fatty acid and to a significant decrease (75%) in glucose oxidation. Importantly, individual analysis of gene clusters from the islets of all donors revealed the induction of genes involved in inflammation and immunity, which provides further evidence that FFA are risk factors for the development of type 2 diabetes. In summary, our data indicate that chronic exposure of human islets to FFA activates inflammatory and metabolic pathways that lead to oxidative stress, reduced b-cell insulin content, and inhibition of GSIS.

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“…Free fatty acid metabolism in obesity has, therefore, been the subject of many studies over the last thirty years. Unfortunately, conflicting conclusions regarding several aspects of FFA metabolism have appeared, including the antilipolytic effectiveness ofinsulin in obesity (1,2), the relationship of FFA release to the amount of body fat (3)(4)(5), and the lipolytic responsiveness of obese individuals to catecholamines (6)(7)(8). These potential differences in FFA metabolism between lean and obese humans may be of considerable importance in that they reflect either abnormalities of adipose tissue or of the body's ability to hormonally regulate adipose tissue lipolysis.…”

Section: Introductionmentioning

confidence: 99%

Influence of body fat distribution on free fatty acid metabolism in obesity.

Jensen¹,

Haymond²,

Rizza³

et al. 1989

J. Clin. Invest.

628

380

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In order to determine whether differences in body fat distribution result in specific abnormalities of free fatty acid (FFA) metabolism, palmitate turnover, a measure of systemic adipose tissue lipolysis, was measured in 10 women with upper body obesity, 9 women with lower body obesity, and 8 nonobese women under overnight postabsorptive (basal), epinephrine stimulated and insulin suppressed conditions. Results: Upper body obese women had greater (P < 0.005) basal palmitate turnover than lower body obese or nonobese women (2.8±0.2 vs. 2.1±0.2 vs. 1.8±0.2 Mmolt kg lean body mass (LBM)-1 * min-, respectively), but a reduced (P < 0.05) net lipolytic response to epinephrine (59±7 vs. 79±5 vs. 81±7 Mmol palmitate/kg LBM, respectively). Both types of obesity were associated with impaired suppression of FFA turnover in response to euglycemic hyperinsulinemia compared to nonobese women (P < 0.005). These specific differences in FFA metabolism may reflect adipocyte heterogeneity, which may in turn affect the metabolic abberations associated with different types of obesity. These findings emphasize the need to characterize obese subjects before studies.

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Lipid mobilization in relation to body composition in man

Cited by 91 publications

References 29 publications

Effects of pair-feeding and growth hormone treatment on obese transgenic rats

Effects of pair-feeding and growth hormone treatment on obese transgenic rats

Ex vivo transcriptional profiling of human pancreatic islets following chronic exposure to monounsaturated fatty acids

Influence of body fat distribution on free fatty acid metabolism in obesity.

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