Adrenal Function and the Effect of a High-Fat Diet on C57BL/6J and C57BL/6J-ob/ob Mice

Abstract

In C57BL/6J mice and the ob/+ and ob/ob mutants total plasma corticosterone levels were found to be statistically different. In C57BL/6J mice the level was 1.9 +/- 0.2 mug/100 ml plasma, in ob/+ mice 8.6 +/- 1.6 mug/100 ml and in ob/ob mice 13.7 +/- 1.5 mug/100 ml. The percentage of protein-bound corticosterone as well as the free endogenous corticosterone levels were also different. Feeding a high-fat diet to young C57BL/6J and C57BL/6J-ob/ob mice for a period of 4 weeks had no effect upon blood glucose, plasma insulin and plasma corticosterone levels. The significantly higher increase in body weight of the high-fat diet groups of both lines of mice was mainly due to fat cell hypertrophy.

Apolipoprotein A-IV is regulated by nutritional and metabolic stress: involvement of glucocorticoids, HNF-4α, and PGC-1α

“…Thus, these mice are often used as a model of type II diabetes (46). Interestingly, ob/ob mice have glucocorticoid levels 14-fold greater than controls, and adrenalectomy of these mice leads to a reversal of obesity (47,48). In this study, liver apoA-IV mRNA and plasma protein levels were greatly increased in 12 week old ob/ob mice.…”

Hormonal regulation of hepatic soluble phosphatidate phosphohydrolase

“…The results thus lend support to the hypothesis that under most of the above-mentioned conditions adrenocortical steroids may be the mediators of the effects on phosphatidate phosphohydrolase. This may have some bearing on the enhanced synthesis of hepatic triacylglycerols in certain stress states (e.g., ethanol loading, partial hepatectomy, laparotomy) and presumably also in obesity, at least in genetically obese mice, in which there is hyperfunction of the adrenal cortex [35] and increased activity of phosphatidate phosphohydrolase [32].…”

Leptin directly regulates bone cell function in vitro and reduces bone fragility in vivo

“…Conversely in the ob/ob mouse, insulin concentrations are 10-fold higher than in wild-type controls (Herberg & Kley 1975), which could contribute to its high bone mass. Systemic administration of leptin is associated with reduced insulin concentrations (Kulkarni et al 1997, Scrocchi et al 1997, Seufert et al 1999, Shimomura et al 1999, so the positive skeletal effects found in the present in vivo study in the face of these changes emphasise the direct effects of leptin on bone.…”