Energy intake-independent modulation of triglyceride metabolism by glucocorticoids in the rat

Abstract

This study aimed to dissociate the peripheral effects of adrenalectomy (ADX) on triglyceride (TG) metabolism from those it exerts centrally on energy intake and to determine the impact of diet composition therein. Rats were fed either rodent chow or a diet high in sucrose and fat (HSF) and were adrenalectomized or left intact and pair fed to the ADX animals. Liver TG content, an index of hepatic TG production, was not affected by ADX, but was increased twofold by the HSF diet. ADX decreased the rate of hepatic TG secretion by 41% in chow-fed but not in HSF-fed animals. Triglyceridemia and postheparin plasma lipase activities remained largely unchanged by treatments. ADX decreased insulinemia fivefold in chow-fed rats, but less so in HSF-fed animals. Likewise, subcutaneous and visceral adipose depots were 40-60% smaller in ADX than in intact pair-fed rats given chow, but the effect of ADX was dampened by consumption of the HSF diet. Although smaller, adipose tissues of ADX rats maintained a higher activity of lipoprotein lipase (LPL) than those of intact pair-fed rats, whereas muscle LPL was decreased. The study confirms that in the presence of reduced energy intake, corticosterone contributes to the maintenance of adipose stores and that the consequences of its absence tend to be attenuated when a high-energy diet is fed. The study further shows that, contrary to ad libitum feeding conditions, most determinants of TG metabolism, such as hepatic TG stores, triglyceridemia, postheparin plasma LPL, and adipose tissue LPL, are minimally affected by glucocorticoids when consumption of a high-energy diet is restricted, suggesting that glucocorticoids affect TG metabolism mostly indirectly through their central action on ingestive behavior.

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“…Similar results were observed in another study using adrenalectomized rats with diet-induced obesity demonstrating the effects of GC action on plasma and liver triglyceride levels, plasma insulin, and adipose tissue weight [85]. These effects appear to be minimized when there is restriction on high-energy diet [86], suggesting they may be exerted via mediating the central ingestive behavior. These findings highlight the central role of GCs in the development of obesity and other features of the Metabolic Syndrome.…”

Ghrelin regulates mitochondrial-lipid metabolism gene expression and tissue fat distribution in liver and skeletal muscle

“…In particular, reported prolactin effects on liver and white adipose tissue lipogenic gene expression and function are opposite to those observed after ghrelin treatment in the current study (1). In addition, excess glucocorticoids are not reported to exert independent effects on hepatic lipogenesis and lipid deposition (14,29,54), whereas most (16,18,30), although not all (55), reports agree on their suppressive or null effect on skeletal muscle mitochondrial function. Thus, taken together, the above observations do not support a major role of additional hypophyseal hormonal changes in observed metabolic effects.…”

Obesity induced by a pair-fed high fat sucrose diet: methylation and expression pattern of genes related to energy homeostasis

“…Other studies have reported comparable results in rodents fed ad libitum with a similar diet [3], but apparently never within a pair-fed model. In fact, a pair-feeding model of HFS diet was performed in Sprague-Dawley rats, although no changes in body weight gain were observed [17]. The strongest evidence of the experimental hypothesis comes from rodent studies in which a high-fat (HF) diet induced obesity independently of total energy intake [18,19].…”