scholarly journals Progressive Adipocyte Hypertrophy in Aquaporin-7-deficient Mice

2005 ◽  
Vol 280 (16) ◽  
pp. 15493-15496 ◽  
Author(s):  
Mariko Hara-Chikuma ◽  
Eisei Sohara ◽  
Tatemitsu Rai ◽  
Masahito Ikawa ◽  
Masaru Okabe ◽  
...  
Keyword(s):  
Body Fat ◽  
Fat Mass ◽  
Body Fat Mass ◽  
Wild Type ◽  
Adipocyte Volume ◽  
Aquaporin 7 ◽  
Adipocyte Hypertrophy ◽  
Adipocyte Plasma Membranes ◽  
Deficient Mice ◽  
Glycerol Permeability

Aquaporin-7 (AQP7) is a water/glycerol transporting protein expressed in adipocyte plasma membranes. We report here remarkable age-dependent hypertrophy in adipocytes in AQP7-deficient mice. Wild type and AQP7 null mice had similar growth at 0–16 weeks as assessed by body weight; however, by 16 weeks AQP7 null mice had 3.7-fold increased body fat mass. Adipocytes from AQP7 null mice of age 16 weeks were greatly enlarged (diameter 118 μm) compared with wild type mice (39 μm). Adipocytes from AQP7 null mice also accumulated excess glycerol (251versus86 nmol/mg of protein) and triglycerides (3.4versus1.7 μmol/mg of protein). In contrast, at age 4 weeks, adipocyte volume and body fat mass were comparable in wild type and AQP7 null mice. To investigate the mechanism(s) responsible for the progressive adipocyte hypertrophy, glycerol permeability and fat metabolism were studied in adipocytes isolated from the younger mice. Plasma membrane glycerol permeability measured by [14C]glycerol uptake was 3-fold reduced in AQP7-deficient adipocytes. However, adipocyte lipolysis, measured by free fatty acid release and hormone-sensitive lipase activity, and lipogenesis, measured by [14C]glucose incorporation into triglycerides, were not affected by AQP7 deletion. These data suggest that adipocyte hypertrophy in AQP7 deficiency results from defective glycerol exit and consequent accumulation of glycerol and triglycerides. Increasing AQP7 expression/function in adipocytes may reduce adipocyte volume and fat mass in obesity.

scholarly journals Increased energy expenditure and leptin sensitivity account for low fat mass in myostatin-deficient mice

2011 ◽  
Vol 300 (6) ◽  
pp. E1031-E1037 ◽  
Author(s):  
Sun Ju Choi ◽  
Zipora Yablonka-Reuveni ◽  
Karl J. Kaiyala ◽  
Kayoko Ogimoto ◽  
Michael W. Schwartz ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Body Mass ◽  
Body Fat ◽  
Fat Mass ◽  
Body Fat Mass ◽  
Low Fat ◽  
Total Body Mass ◽  
Leptin Sensitivity ◽  
Deficient Mice

Myostatin deficiency causes dramatically increased skeletal muscle mass and reduced fat mass. Previously, myostatin-deficient mice were reported to have unexpectedly low total energy expenditure (EE) after normalizing to body mass, and thus, a metabolic cause for low fat mass was discounted. To clarify how myostatin deficiency affects the control of body fat mass and energy balance, we compared rates of oxygen consumption, body composition, and food intake in young myostatin-deficient mice relative to wild-type (WT) and heterozygous (HET) controls. We report that after adjusting for total body mass using regression analysis, young myostatin-deficient mice display significantly increased EE relative to both WT (+0.81 ± 0.28 kcal/day, P = 0.004) and HET controls (+0.92 ± 0.31 kcal/day, P = 0.005). Since food intake was not different between groups, increased EE likely accounts for the reduced body fat mass (KO: 8.8 ± 1.1% vs. WT: 14.5 ± 1.3%, P = 0.003) and circulating leptin levels (KO: 0.7 ± 0.2 ng/ml vs. WT: 1.9 ± 0.3 ng/ml, P = 0.008). Interestingly, the observed increase in adjusted EE in myostatin-deficient mice occurred despite dramatically reduced ambulatory activity levels (−50% vs. WT, P < 0.05). The absence of hyperphagia together with increased EE in myostatin-deficient mice suggests that increased leptin sensitivity may contribute to their lean phenotype. Indeed, leptin-induced anorexia (KO: −17 ± 1.2% vs. WT: −5 ± 0.3%) and weight loss (KO: −2.2 ± 0.2 g vs. WT: −1.6 ± 0.1, P < 0.05) were increased in myostatin-deficient mice compared with WT controls. We conclude that increased EE, together with increased leptin sensitivity, contributes to low fat mass in mice lacking myostatin.

scholarly journals In vivo evidence for unidentified leptin-induced circulating factors that control white fat mass

2015 ◽  
Vol 309 (12) ◽  
pp. R1499-R1511 ◽  
Author(s):  
Ruth B. S. Harris
Keyword(s):  
Cell Size ◽  
Body Fat ◽  
Fat Mass ◽  
Leptin Receptor ◽  
Recipient Mouse ◽  
Body Fat Mass ◽  
Energy Status ◽  
Wild Type ◽  
Cell Size Distribution ◽  
Leptin Receptors

Fat transplants increase body fat mass without changing the energy status of an animal and provide a tool for investigating control of total body fat. Early transplant studies found that small pieces of transplanted fat took on the morphology of the transplant recipient. Experiments described here tested whether this response was dependent upon expression of leptin receptors in either transplanted fat or the recipient mouse. Fat from leptin receptor deficient db/db mice or wild-type mice was placed subcutaneously in db/db mice. After 12 wk, cell size distribution in the transplant was the same as in endogenous fat of the recipient. Thus, wild-type fat cells, which express leptin receptors, were enlarged in a hyperleptinemic environment, indicating that leptin does not directly control adipocyte size. By contrast, db/db or wild-type fat transplanted into wild-type mice decreased in size, suggesting that a functional leptin system in the recipient is required for body fat mass to be controlled. In the final experiment, wild-type fat was transplanted into a db/db mouse parabiosed to either another db/db mouse to an ob/ob mouse or in control pairs in which both parabionts were ob/ob mice. Transplants increased in size in db/db–db/db pairs, decreased in db/db–ob/ob pairs and did not change in ob/ob-ob/ob pairs. We propose that leptin from db/db parabionts activated leptin receptors in their ob/ob partners. This, in turn, stimulated release of unidentified circulating factors, which travelled back to the db/db partner and acted on the transplant to reduce fat cell size.

Novel genes on rat chromosome 10 are linked to body fat mass, preadipocyte number and adipocyte size

2016 ◽  
Vol 11 (S 01) ◽  
Author(s):  
A Weingarten ◽  
L Turchetti ◽  
K Krohn ◽  
M Kern ◽  
I Klöting ◽  
...  
Keyword(s):  
Body Fat ◽  
Fat Mass ◽  
Body Fat Mass ◽  
Adipocyte Size ◽  
Chromosome 10 ◽  
Novel Genes

1019-P: Glucagon-Like Peptide-1 Receptor Agonists Predominantly Reduce Body Fat Mass in Patients with Type 2 Diabetes

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1019-P
Author(s):  
YUKI FUJITA ◽  
SODAI KUBOTA ◽  
HITOSHI KUWATA ◽  
DAISUKE YABE ◽  
YOSHIYUKI HAMAMOTO ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Body Fat ◽  
Fat Mass ◽  
Body Fat Mass ◽  
Receptor Agonists ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals High percent body fat mass predicts lower risk of cardiac events in patients with heart failure: an explanation of the obesity paradox

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Katsuhiko Ohori ◽  
Toshiyuki Yano ◽  
Satoshi Katano ◽  
Hidemichi Kouzu ◽  
Suguru Honma ◽  
...  
Keyword(s):  
Heart Failure ◽  
Body Fat ◽  
Fat Mass ◽  
Cardiac Event ◽  
Muscle Wasting ◽  
Obesity Paradox ◽  
Percent Body Fat ◽  
Body Fat Mass ◽  
Cardiac Events ◽  
Kaplan Meier

Abstract Background Although high body mass index (BMI) is a risk factor of heart failure (HF), HF patients with a higher BMI had a lower mortality rate than that in HF patients with normal or lower BMI, a phenomenon that has been termed the “obesity paradox”. However, the relationship between body composition, i.e., fat or muscle mass, and clinical outcome in HF remains unclear. Methods We retrospectively analyzed data for 198 consecutive HF patients (76 years of age; males, 49%). Patients who were admitted to our institute for diagnosis and management of HF and received a dual-energy X-ray absorptiometry scan were included regardless of left ventricular ejection fraction (LVEF) categories. Muscle wasting was defined as appendicular skeletal muscle mass index < 7.0 kg/m2 in males and < 5.4 kg/m2 in females. Increased percent body fat mass (increased FM) was defined as percent body fat > 25% in males and > 30% in females. Results The median age of the patients was 76 years (interquartile range [IQR], 67–82 years) and 49% of them were male. The median LVEF was 47% (IQR, 33–63%) and 33% of the patients had heart failure with reduced ejection fraction. Increased FM and muscle wasting were observed in 58 and 67% of the enrolled patients, respectively. During a 180-day follow-up period, 32 patients (16%) had cardiac events defined as cardiac death or readmission by worsening HF or arrhythmia. Kaplan-Meier survival curves showed that patients with increased FM had a lower cardiac event rate than did patients without increased FM (11.4% vs. 22.6%, p = 0.03). Kaplan-Meier curves of cardiac event rates did not differ between patients with and those without muscle wasting (16.5% vs. 15.4%, p = 0.93). In multivariate Cox regression analyses, increased FM was independently associated with lower cardiac event rates (hazard ratio: 0.45, 95% confidence interval: 0.22–0.93) after adjustment for age, sex, diabetes, muscle wasting, and renal function. Conclusions High percent body fat mass is associated with lower risk of short-term cardiac events in HF patients.

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