Effects of aldosterone on lipid metabolism and renal oxygen consumption in the rat

Abstract

The plasma level of free fatty acids (FFA) in adrenalectomized rats increases by 50% after treatment with aldosterone (2 microng/100 g rat). Lipolytic activity in peripheral fat tissue is lowered after adrenalectomy and doubles after in vivo administration of aldosterone to adrenalectomized rats (measured as free fatty acid release in vitro from epididymal fat tissue). Lypolysis of adipose tissue stimulated by the in vitro presence of ACTH also increases after in vivo administration of aldosterone. Incorporation of intravenously administered label from U-14C-palmitate into total extractable lipid of renal tissue is augmented 3 h after aldosterone administration to adrenalectomized rats, while no increase of the radioactivity is observed in total lipid from liver tissue. Treatment with aldosterone does not affect the total lipid content of kidney or liver in adrenalectomized rats. The oxygen consumption rate of kidney cortex slices with lactate, beta-hydroxybuterate or acetoacetate as substrates is lowered after in vivo administration of aldosterone to adrenalectomized rats. With slccinate, however, the respiratory rate of kidney slices increases after aldosterone treatment of adrenalectomized rats, the ouabain-sensitive respiration being more affected than the ouabain-insensitive respiration. An interpretation of the O2 consumption data implicating competition of lipid metabolism for CoA-SH is discussed.

Metabolic cross talk between the colon and the periphery: implications for insulin sensitivity

“…It is possible therefore that aldosterone itself might be the primary cause of insulin resistance, although currently there is little evidence in the literature for a direct causal link. In animal studies aldosterone treatment has been found to increase plasma NEFA levels, consistent with an effect on AT lipolysis (Kirsten et al 1977), and aldosterone added to human adipocytes in vitro reduces insulin-dependent glucose uptake by 30% (Kraus et al 2005). The relationship between aldosterone and glucose metabolism is poorly understood, but in the light of recent findings linking both primary and secondary aldosteronism with insulin resistance and hyperinsulinaemia, more work to elucidate this metabolic link is warranted.…”

Leptin alters energy intake and fat mass but not energy expenditure in lean subjects

“…It was only associated with the reduction observed in aldosterone levels in study 3, which was not verified in study 4, where dose adjustments were performed to prevent too much body weight loss. Given that aldosterone has rather lipolytic properties 55 , the transient, increased serum FFA may have an inhibitory effect on aldosterone secretion as a part of a compensatory mechanism. Furthermore, even though we see some small changes in FFA with leptin, these are not proportional to the changes in fat mass, suggesting that they may account for some minor but not all of leptin’s effects on body weight/fat mass that are probably due to the decreasing energy intake.…”

The long term microbiota and metabolic status in patients with colorectal cancer after curative colon surgery

“…the decreased glucagon-like peptide 1 (GLP-1) concentrations secreted by endocrine L-cells in the distal gut [4,17], 3.) the secondary aldosteronism [20,21]. Furthermore, the finding that RH patients, rather than LAR patients, had a higher serum fasting glucose and higher occurrence of metabolic syndrome when compared with those of control imply that proximal colon may play an important role in glucose control.…”