Dataset Information

Hepatic expression of cell death-inducing DFFA-like effector C in obese subjects is reduced by marked weight loss.

ABSTRACT: The hepatic expression of the cell death-inducing DNA fragmentation factor A-like effector family (CIDEA, CIDEB, and CIDEC) genes is markedly upregulated in mouse models of obesity. We evaluated the expression of CIDE genes in liver of obese human subjects undergoing gastric bypass surgery (GBS), at the time of surgery and again 1 year later when subjects had lost 37.6 +/- 1.4% of their initial body weight. At the time of GBS, the expression of CIDEA (r(2) = 0.20, P = 0.04) and CIDEC (r(2) = 0.32, P = 0.01) was strongly correlated with BMI, whereas CIDEB was not (r(2) = 0.01, P = 0.81). One year after surgery, CIDEC expression had declined over 60% (P = 0.02), whereas CIDEA expression did not change (P = 0.20). These data demonstrate that, consistent with previous studies conducted in rodents, hepatic expression of CIDEA and CIDEC, but not CIDEB, is increased in obese humans. Moreover, the hepatic expression of CIDEC is downregulated by marked weight loss.

SUBMITTER: Hall AM

PROVIDER: S-EPMC2957480 | biostudies-literature | 2010 Feb

REPOSITORIES: biostudies-literature

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Hepatic expression of cell death-inducing DFFA-like effector C in obese subjects is reduced by marked weight loss.

Hall Angela M AM Brunt Elizabeth M EM Klein Samuel S Finck Brian N BN

Obesity (Silver Spring, Md.) 20090806 2

The hepatic expression of the cell death-inducing DNA fragmentation factor A-like effector family (CIDEA, CIDEB, and CIDEC) genes is markedly upregulated in mouse models of obesity. We evaluated the expression of CIDE genes in liver of obese human subjects undergoing gastric bypass surgery (GBS), at the time of surgery and again 1 year later when subjects had lost 37.6 +/- 1.4% of their initial body weight. At the time of GBS, the expression of CIDEA (r(2) = 0.20, P = 0.04) and CIDEC (r(2) = 0.3 ...[more]

PMID: 19661960

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Project description:OBJECTIVE: To compare the effects of weight loss on visceral and subcutaneous abdominal fat, liver and pancreas lipid content and to test the effects of these changes on metabolic improvement observed after weight loss. DESIGN: Weight-loss program designed to achieve a loss of 7-10% of the initial weight. SUBJECTS: 24 obese subjects (13 males and 11 females) with age ranging from 26 to 69 years and body mass index (BMI) 30.2-50.5 kg m(-2). MEASUREMENTS: weight, BMI, waist circumference, body composition as assessed by dual-energy X-ray absorptiometry, metabolic variables, leptin, adiponectin, visceral and subcutaneous abdominal fat, liver and pancreas lipid content as assessed by magnetic resonance were evaluated before and after weight loss achieved by hypocaloric diet. RESULTS: After a mean body weight decrease of 8.9%, BMI, waist circumference, fat mass, all metabolic variables, homeostasis model assessment of insulin resistance (HOMA), alanine amino transferase, gamma glutamyl transpeptidase, high-sensitivity C-reactive protein (hs-CRP) and leptin, but not adiponectin and high-density lipoprotein-cholesterol, significantly decreased (all P<0.01). Visceral and subcutaneos abdominal fat, liver and pancreas lipid content significantly decreased (all P<0.01). Percent changes in liver lipid content were greater (84.1±3%) than those in lipid pancreas content (42.3±29%) and visceral abdominal fat (31.9±15.6%). After weight loss, percentage of subjects with liver steatosis decreased from 75 to 12.5%. Insulin resistance improvement was predicted by changes in liver lipid content independently of changes in visceral fat, pancreas lipid content, systemic inflammation, leptin and gender. CONCLUSION: Moderate weight loss determines significant decline in visceral abdominal fat, lipid content in liver and pancreas. Reduction of liver lipid content was greater than that of pancreas lipid content and visceral fat loss. Liver lipid content is the strongest predictor of insulin resistance improvement after weight loss.

Project description:Background. Differential gene expression in adipose tissue during diet-induced weight loss followed by a weight stability period is not well characterized. Markers of these processes may provide a deeper understanding of the underlying mechanisms. Objective. To identify differentially expressed genes in human adipose tissue during weight loss and weight maintenance after weight loss. Design. RNA from subcutaneous abdominal adipose tissue from nine obese subjects was obtained and analyzed at baseline, after weight reduction on a low calorie diet (LCD), and after a period of group therapy in order to maintain weight stability. Results. Subjects lost 18.8 + 5.4% of their body weight during the LCD and maintained this weight during group therapy. Insulin sensitivity (HOMA) improved after weight loss with no further improvement during weight maintenance. Cyclin-dependent kinase inhibitor 2B (CDKN2B) and JAZF zinc finger 1 (JAZF1), associated with type 2 diabetes, were downregulated. We could also confirm the downregulation of candidates for obesity and related traits, such as tenomodulin (TNMD) and matrix metallopeptidase 9 (MMP9), with weight loss. The expression of other candidates, such as cell death-inducing DFFA-like effector A (CIDEA) and stearoyl-CoA desaturase (SCD) were upregulated during weight loss but returned to baseline levels during weight maintenance. Conclusion. Genes in the adipose tissue are differentially expressed during weight loss and weight maintenance after weight loss. Genes that show sustained regulation may be of potential interest as markers of the beneficial effects of weight loss whereas others seem to be primarily involved in the process of weight loss itself. Nine participants were prescribed a low calorie diet (LCD) containing 1200 kcal/day for approximately three months (101 ± 26 days). Following the weight reduction phase the participants attended a six month follow-up period (167 ± 37 days). By protocol design, subjects were eligible to enter the study if they had lost at least 10% of their initial body weight during the LCD-period and maintained this weight (+5%) after group therapy. Subcutaneous adipose tissue samples were obtained at three time-points: (i) at baseline, (ii) after weight reduction when subjects were no longer losing weight, and (iii) after the group therapy weight maintenance phase.

Dataset Information

Hepatic expression of cell death-inducing DFFA-like effector C in obese subjects is reduced by marked weight loss.

Publications

Hepatic expression of cell death-inducing DFFA-like effector C in obese subjects is reduced by marked weight loss.

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