open access

https://hdl.handle.net/2115/43189

Calcium deficiency in the early stages after weaning is associated with the enhancement of a low level of adrenaline-stimulated lipolysis and reduction of adiponectin release in isolated rat mesenteric adipocytes

英語

2010-07

Elsevier

Metabolism

59(7)

951-958

Dysregulation of visceral adipocytes increases the incidence of metabolic syndrome. Higher production of non-esterified fatty acid (NEFA) and changes in adipocytokine release may trigger insulin resistance. Many studies have suggested that calcium (Ca) deficiency is associated with insulin resistance; however, the mechanisms are poorly understood. We examined the effects of Ca deficiency on adrenaline-induced lipolysis and adipocytokine release in the early stages after weaning using freshly isolated adipocytes from mesenteric fat tissue of 3-week-old male Sprague-Dawley rats fed a normal-Ca (5 g/kg diet) or low Ca (1 g/kg diet) diet for 4 weeks. The release rate of NEFA in the mesenteric adipocytes after stimulation with a low level of adrenaline (0.2 μg/mL) was much higher in the Ca-deficient group than in the control group. In contrast, adiponectin release in the mesenteric fat cells was lower in Ca-deficient rats. Leptin and TNF-α secretion showed a similar tendency without significant inter-group differences, and MCP-1 release was not affected by Ca deficiency. We found that Ca deficiency reduced the average size of fat cells through a large increase in the number of cells slightly smaller than the average size, which may be associated with the changes in the properties of the mesenteric adipose tissue. Our present results suggest that a low intake of Ca in the early stages after weaning is associated with changes in the properties of mesenteric adipocytes, which may be linked to insulin resistance in the future.

学術雑誌論文

Accepted Manuscript

0026-0495