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

Dysregulation of visceral adipocytes increases the incidence of metabolic syndrome. Higher production of nonesterified fatty acid 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 nonesterified fatty acid 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 tumor necrosis factor–α secretion showed a similar tendency without significant intergroup differences, and monocyte chemoattractant protein–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.