a1 Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, 5° andar, Avenue 28 de Setembro, 87, Rio de Janeiro, RJ 20551-030, Brazil
It is known that Ca therapy may have anti-obesity effects. Since early weaning leads to obesity, hyperleptinaemia and insulin resistance, we studied the effect of dietary Ca supplementation in a rat model. Lactating rats were separated into two groups: early weaning (EW) – dams were wrapped with a bandage to interrupt lactation in the last 3 d of lactation and control (C) – dams whose pups had free access to milk during the entire lactation period (21 d). At 120 d, EW and C offspring were subdivided into four groups: (1) C, received standard diet; (2) CCa, received Ca supplementation (10 g of calcium carbonate/kg of rat chow); (3) EW, received standard diet; (4) EWCa, received Ca supplementation similar to CCa. The rats were killed at 180 d. The significance level was at P < 0·05. Adult EW offspring displayed hyperphagia (28 %), higher body weight (9 %) and adiposity (77 %), hyperleptinaemia (twofold increase), hypertriacylglycerolaemia (64 %), hyperglycaemia (16 %), higher insulin resistance index (38 %) and higher serum 25-hydroxyvitamin D3 (fourfold increase), but lower adiponectinaemia:adipose tissue ratio (44 %). In addition, they showed Janus tyrosine kinase 2 and phosphorylated signal transducer and activator of transcription 3 underexpression in hypothalamus (36 and 34 %, respectively), suggesting leptin resistance. Supplementation of Ca for 2 months normalised these disorders. The EW group had no change in serum insulin, thyroxine or triiodothyronine, and Ca treatment did not alter these hormones. In conclusion, we reinforced that early weaning leads to late development of some components of the metabolic syndrome and leptin resistance. Dietary Ca supplementation seems to protect against the development of endocrine and metabolic disorders in EW offspring, maybe through vitamin D inhibition.
(Received December 14 2010)
(Revised May 25 2011)
(Accepted June 20 2011)
(Online publication November 09 2011)
Abbreviations: 11β-HSD-1, 11β-hydroxysteroid dehydrogenase-1; BW, body weight; C, control; EW, early weaning; HOMA-IR, homeostasis model assessment of insulin resistance; JAK2, Janus tyrosine kinase 2; pJAK2, phosphorylated Janus tyrosine kinase 2; pSTAT3, phosphorylated signal transducer and activator of transcription 3; SOCS3, suppressor of cytokine signalling 3; VFM, visceral fat mass