Determinants of leptin gene expression in fat depots of lean mice

Zhang, Yiying; Guo, Kai; Díaz, P.; Heo, Moonseong; Leibel, Rudolph L.

doi:10.1152/ajpregu.00392.2001

Cited by 114 publications

(91 citation statements)

References 60 publications

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“…It is well known that leptin levels strongly correlate with the amount of lipid 37,38 and its release is proportional to adipocyte volume. 36 Compared to the uninfected control, the virus increases differentiation of 3T3-L1 cells, 11 resulting in greater proportion of adipocytes and the lipid content. As adipocytes, but not preadipocytes secrete leptin, it would be misleading to compare leptin secretion of two groups containing unequal number or size of adipocytes.…”

Section: Discussionmentioning

confidence: 98%

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Adipogenic human adenovirus-36 reduces leptin expression and secretion and increases glucose uptake by fat cells

et al. 2006

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Objective: Human adenovirus Ad-36 causes adiposity in animal models and enhances differentiation and lipid accumulation in human and 3T3-L1 preadipocytes, which may, in part, explain the adipogenic effect of Ad-36. We determined the consequences of Ad-36 infection on leptin and glucose metabolism in fat cells. Design: 3T3-L1 preadipocytes were used to determine the effect of infection by human adenoviruses Ad-36, Ad-2, Ad-9 and Ad-37 on leptin secretion and lipid accumulation. Rat primary adipocytes were used to determine the effect of Ad-36 infection on leptin secretion and glucose uptake in vitro. Furthermore, the effect of Ad-36 on expressions of leptin and selected genes of de novo lipogenesis pathway of visceral adipose tissue were compared ex vivo, between Ad-36 infected and uninfected control rats. Results: Ad-36 suppressed the expression of leptin mRNA in 3T3-L1 cells by approximately 58 and 52% on days 3 and 5 postinfection, respectively. Leptin release normalized to cellular lipid content was 51% lower (Po0.002) in the Ad-36 infected 3T3-L1 cells. Lipid accumulation was significantly greater and leptin secretion was lower for the 3T3-L1 cells infected with other human adenoviruses Ad-9, Ad-36, or Ad-37. Whereas, human adenovirus Ad-2 did not influence cellular lipid accumulation or the leptin release. In rat primary adipocytes, Ad-36 reduced leptin release by about 40% in presence of 0.48 (Po0.01) or 1.6 nM insulin (Po0.05) and increased glucose uptake by 93% (Po0.001) or 18% (Po0.05) in presence of 0 or 0.48 nM insulin, respectively. Next, the adipose tissue of Ad-36 infected rats showed two to fivefold lower leptin mRNA expression, and 1.6-to 21-fold greater expressions for acetyl Co-A carboxylase-1 and 1.2-to 6.3-fold greater expressions for fatty acid synthase, key genes of de novo lipogenesis, compared to the uninfected weight and adiposity matched controls. Conclusion: The in vitro and ex vivo studies show that Ad-36 modulates adipocyte differentiation, leptin production and glucose metabolism. Whether such a modulation contributes to enhanced adipogenesis and consequent adiposity in Ad-36 infected animals or humans needs to be determined.

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Section: Discussionmentioning

confidence: 98%

“…36 Considering the continued relative suppression of leptin expression by Ad-36 on day 5 (Figure 2), and to allow its adequate production and release, leptin release by 3T3-L1 cells was determined on day 5 post-inoculation (Experiment 2). Leptin levels were within the detectable range of the standard curve.…”

Section: Discussionmentioning

confidence: 99%

Adipogenic human adenovirus-36 reduces leptin expression and secretion and increases glucose uptake by fat cells

et al. 2006

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“…It has been postulated as a sensor of fat mass and a hormonal signal that exerts its effect on energy regulation through its hypothalamic receptor (15,16). Because the adipocyte is the only source of ob gene products, serum leptin level has a strong positive association with the amount of body fat and adipocyte leptin mRNA in humans as in rodents (35)(36)(37). Several studies have examined serum leptin level and future weight gain, but few have examined change in regional adiposity (17,38,39).…”

Section: Discussionmentioning

confidence: 99%

Insulin, C-Peptide, and Leptin Concentrations Predict Increased Visceral Adiposity at 5- and 10-Year Follow-Ups in Nondiabetic Japanese Americans

et al. 2005

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We prospectively examined the relationship between leptin and markers of insulin resistance and secretion and future visceral adipose tissue accumulation. In this study, 518 nondiabetic Japanese-American men and women underwent the following measurements at baseline and at 5-and 10-year follow-ups: plasma glucose and insulin measured after an overnight fast and during a 75-g oral glucose tolerance test, insulin secretion ratio (ISR) [(30-min insulin ؊ fasting insulin)/30-min glucose], fasting C-peptide levels, plasma leptin (baseline only), and fat areas (intra-abdominal and subcutaneous) measured by computed tomography. Predictors of future intra-abdominal fat (IAF) were determined using multiple linear regression. Fasting insulin and C-peptide levels at baseline were significantly associated with IAF area at 5 years (coefficient ‫؍‬ 0.041, P ‫؍‬ 0.001 and coefficient ‫؍‬ 1.283, P < 0.001, respectively) and 10 years (coefficient ‫؍‬ 0.031, P ‫؍‬ 0.020 and coefficient ‫؍‬ 0.221, P ‫؍‬ 0.035, respectively). ISR was not significantly associated with IAF at 5 or 10 years. Leptin level at baseline was positively associated with IAF at 5 years (coefficient ‫؍‬ 0.055, P ‫؍‬ 0.002) and 10 years (coefficient ‫؍‬ 0.059, P ‫؍‬ 0.003). In conclusion, higher levels of fasting insulin, C-peptide, and circulating leptin level predicted visceral fat accumulation independent from subcutaneous fat accumulation in nondiabetic Japanese-American men and women in both short-term (5 years) and long-term (10 years) followup. Diabetes 54: [985][986][987][988][989][990] 2005

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“…It has also been discussed whether the regional difference in leptin gene expression might be due partly to a difference in mean fat cell volume (8). In lean mice, depot-specific differences in leptin gene expression are mainly related to the volumes of the constituent adipocytes (25).…”

Section: Discussionmentioning

confidence: 99%

Comparison of leptin gene expression in different adipose tissues in children and adults

Schoof

Stuppy²,

Harig³

et al. 2004

European Journal of Endocrinology

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Objective: Adipose tissue displays depot-specific metabolic properties and a predominant gene expression of leptin in subcutaneous tissue. The aim of the study was to evaluate leptin mRNA expression in various adipose tissues and to relate it to plasma leptin concentrations. Furthermore, developmental changes in leptin gene expression from childhood to adulthood were examined. Design and methods: Thoracic subcutaneous and intrathoracic adipose tissue specimens were obtained in 22 adults (51-81 years) and 23 children (0.1 -17 years) undergoing cardiac surgery, and abdominal subcutaneous, omental and mesenterial fat specimens were collected from 21 adults (38 -79 years) and 22 children (0.2 -17 years) before abdominal surgery. Preoperative plasma leptin concentrations were measured by RIA. Leptin mRNA expression was quantified by TaqMan real-time PCR.

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Determinants of leptin gene expression in fat depots of lean mice

Cited by 114 publications

References 60 publications

Adipogenic human adenovirus-36 reduces leptin expression and secretion and increases glucose uptake by fat cells

Adipogenic human adenovirus-36 reduces leptin expression and secretion and increases glucose uptake by fat cells

Insulin, C-Peptide, and Leptin Concentrations Predict Increased Visceral Adiposity at 5- and 10-Year Follow-Ups in Nondiabetic Japanese Americans

Comparison of leptin gene expression in different adipose tissues in children and adults

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