The adverse metabolic consequences of obesity are best predicted by the quantity of visceral fat. Excess glucocorticoids produce visceral obesity and diabetes, but circulating glucocorticoid levels are normal in typical obesity. Glucocorticoids can be produced locally from inactive 11-keto forms through the enzyme 11β hydroxysteroid dehydrogenase type 1 (11β HSD-1). We created transgenic mice overexpressing 11β HSD-1 selectively in adipose tissue to an extent similar to that found in adipose tissue from obese humans. These mice had increased adipose levels of corticosterone and developed visceral obesity that was exaggerated by a high-fat diet. The mice also exhibited pronounced insulin-resistant diabetes, hyperlipidemia, and, surprisingly, hyperphagia despite hyperleptinemia. Increased adipocyte 11β HSD-1 activity may be a common molecular etiology for visceral obesity and the metabolic syndrome.

http://science.sciencemag.org/content/sci/294/5549/2166.full.pdf

A Transgenic Model of Visceral Obesity and the Metabolic Syndrome

Adiponectin (ADP) is an adipocyte hormone involved in glucose and lipid metabolism. We detected a rise in ADP in cerebrospinal fluid after intravenous (i.v.) injection, consistent with brain transport. In contrast to leptin, intracerebroventricular (i.c.v.) administration of ADP decreased body weight mainly by stimulating energy expenditure. Full-length ADP, mutant ADP with Cys39 replaced with serine, and globular ADP were effective, whereas the collagenous tail fragment was not. Lep(ob/ob) mice were especially sensitive to i.c.v. and systemic ADP, which resulted in increased thermogenesis, weight loss and reduction in serum glucose and lipid levels. ADP also potentiated the effect of leptin on thermogenesis and lipid levels. While both hormones increased expression of hypothalamic corticotropin-releasing hormone (CRH), ADP had no substantial effect on other neuropeptide targets of leptin. In addition, ADP induced distinct Fos immunoreactivity. Agouti (A(y)/a) mice did not respond to ADP or leptin, indicating the melanocortin pathway may be a common target. These results show that ADP has unique central effects on energy homeostasis.

Adiponectin acts in the brain to decrease body weight

Faithful segregation of replicated chromosomes is essential for maintenance of genetic stability and seems to be monitored by several mitotic checkpoints. Various components of these checkpoints have been identified in mammals, but their physiological relevance is largely unknown. Here we show that mutant mice with low levels of the spindle assembly checkpoint protein BubR1 develop progressive aneuploidy along with a variety of progeroid features, including short lifespan, cachectic dwarfism, lordokyphosis, cataracts, loss of subcutaneous fat and impaired wound healing. Graded reduction of BubR1 expression in mouse embryonic fibroblasts causes increased aneuploidy and senescence. Male and female mutant mice have defects in meiotic chromosome segregation and are infertile. Natural aging of wild-type mice is marked by decreased expression of BubR1 in multiple tissues, including testis and ovary. These results suggest a role for BubR1 in regulating aging and infertility.

/pdf/bubr1-insufficiency-causes-early-onset-of-aging-associated-2v88fumt9g.pdf

BubR1 insufficiency causes early onset of aging-associated phenotypes and infertility in mice.

We present a consolidated view of the complexity and challenges of designing studies for measurement of energy metabolism in mouse models, including a practical guide to the assessment of energy expenditure, energy intake and body composition and statistical analysis thereof. We hope this guide will facilitate comparisons across studies and minimize spurious interpretations of data. We recommend that division of energy expenditure data by either body weight or lean body weight and that presentation of group effects as histograms should be replaced by plotting individual data and analyzing both group and body-composition effects using analysis of covariance (ANCOVA).

/pdf/a-guide-to-analysis-of-mouse-energy-metabolism-3eh72cw9w2.pdf

A guide to analysis of mouse energy metabolism

Skeletal Muscle FOXO1 (FKHR) Transgenic Mice Have Less Skeletal Muscle Mass, Down-regulated Type I (Slow Twitch/Red Muscle) Fiber Genes, and Impaired Glycemic Control

NAGY, TIM R., AND ANNE-LAURE CLAIR. Precision and accuracy of dual-energy X-ray absorptiometry for determining in vivo body composition of mice. Obes Res. 2000;8:392‐398. Objective: To evaluate the precision and accuracy of dualenergy X-ray absorptiometry (DXA) for the measurement of total-bone mineral density (TBMD), total-body bone mineral (TBBM), fat mass (FM), and bone-free lean tissue mass (LTM) in mice. Research Methods and Procedures: Twenty-five male C57BL/6J mice (6 to 11 weeks old; 19 to 29 g) were anesthetized and scanned three times (with repositioning between scans) using a peripheral densitometer (Lunar PIXImus). Gravimetric and chemical extraction techniques (Soxhlet) were used as the criterion method for the determination of body composition; ash content was determined by burning at 600°C for 8 hours. Results: The mean intraindividual coefficients of variation (CV) for the repeated DXA analyses were: TBMD, 0.84%; TBBM, 1.60%; FM, 2.20%; and LTM, 0.86%. Accuracy was determined by comparing the DXA-derived data from the first scan with the chemical carcass analysis data. DXA accurately measured bone ash content (p 5 0.942), underestimated LTM (0.59 6 0.05g, p , 0.001), and overestimated FM (2.19 6 0.06g, p , 0.001). Thus, DXA estimated 100% of bone ash content, 97% of carcass LTM, and 209% of carcass FM. DXA-derived values were then used to predict chemical values of FM and LTM. Chemically extracted FM was best predicted by DXA FM and DXA LTM [FM 52 0.50 1 1.09(DXA FM) 2 0.11(DXA LTM), model r 2 5 0.86, root mean square error (RMSE) 5 0.233 g] and chemically determined LTM by DXA LTM [LTM5 20.14 1 1.04(DXA LTM), r 2 5 0.99, RMSE 5 0.238 g]. Discussion: These data show that the precision of DXA for measuring TBMD, TBBM, FM, and LTM in mice ranges from a low of 0.84% to a high of 2.20% (CV). DXA accurately measured bone ash content but overestimated carcass FM and underestimated LTM. However, because of the close relationship between DXA-derived data and chemical carcass analysis for FM and LTM, prediction equations can be derived to more accurately predict body composition.

Precision and Accuracy of Dual‐Energy X‐ray Absorptiometry for Determining in Vivo Body Composition of Mice

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Precision and Accuracy of Dual‐Energy X‐ray Absorptiometry for Determining in Vivo Body Composition of Mice