title: Calcium supplementation reverts central adiposity, leptin, and insulin resistance in adult offspring programed by neonatal nicotine exposure.
abstract: Obesity is a worldwide epidemic. Calcium influences energy metabolism regulation, causing body weight loss. Because maternal nicotine exposure during lactation programs for obesity, hyperleptinemia, insulin resistance (IR), and hypothyroidism, we decided to evaluate the possible effect of dietary calcium supplementation on these endocrine dysfunctions in this experimental model. Osmotic minipumps containing nicotine solution (N: 6 mg/kg per day for 14 days) or saline (C) were s.c. implanted in lactating rats 2 days after giving birth (P2). At P120, N and C offspring were subdivided into four groups: 1) C - standard diet; 2) C with calcium supplementation (CCa, 10 g calcium carbonate/kg rat chow); 3) N - standard diet; and 4) N with calcium supplementation (NCa). Rats were killed at P180. As expected, N offspring showed higher visceral and total body fat, hyperleptinemia, lower hypothalamus leptin receptor (OB-R) content, hyperinsulinemia, and higher IR index. Also, higher tyrosine hydroxylase (TH) expression (+51%), catecholamine content (+37%), and serum 25-hydroxyvitamin D(3) (+76%) were observed in N offspring. Dietary calcium supplementation reversed adiposity, hyperleptinemia, OB-R underexpression, IR, TH overexpression, and vitamin D. However, this supplementation did not reverse hypothyroidism. In NCa offspring, Sirt1 mRNA was lower in visceral fat (-37%) and higher in liver (+42%). In conclusion, dietary calcium supplementation seems to revert most of the metabolic syndrome parameters observed in adult offspring programed by maternal nicotine exposure during lactation. It is conceivable that the reduction in fat mass per se, induced by calcium therapy, is the main mechanism that leads to the increment of insulin action.
authors.affiliation: Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Avenida 28 de setembro 87, Rio de Janeiro, RJ, Brazil.
authors.forename: J L
authors.initials: JL
authors.lastname: Nobre
authors.forename: P C
authors.initials: PC
authors.lastname: Lisboa
authors.forename: A P
authors.initials: AP
authors.lastname: Santos-Silva
authors.forename: N S
authors.initials: NS
authors.lastname: Lima
authors.forename: A C
authors.initials: AC
authors.lastname: Manhães
authors.forename: J F
authors.initials: JF
authors.lastname: Nogueira-Neto
authors.forename: A
authors.initials: A
authors.lastname: Cabanelas
authors.forename: C C
authors.initials: CC
authors.lastname: Pazos-Moura
authors.forename: E G
authors.initials: EG
authors.lastname: Moura
authors.forename: E
authors.initials: E
authors.lastname: de Oliveira
mesh_terms: D050154:Adiposity / Q000187:drug effects* / Q000235:genetics / Q000502:physiology; D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D001483:Base Sequence; D002136:Calcium, Dietary / Q000008:administration & dosage*; D002395:Catecholamines / Q000378:metabolism; D005260:Female; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology; D020738:Leptin / Q000097:blood* / Q000235:genetics; D008055:Lipids / Q000097:blood; D024821:Metabolic Syndrome / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control; D023421:Models, Animal; D009538:Nicotine / Q000008:administration & dosage*; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D054411:Receptors, Leptin / Q000378:metabolism; D056564:Sirtuin 1 / Q000235:genetics; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D002136:Calcium, Dietary; D002395:Catecholamines; D020738:Leptin; D008055:Lipids; D012333:RNA, Messenger; D054411:Receptors, Leptin; D009538:Nicotine; D014446:Tyrosine 3-Monooxygenase; C488368:Sirt1 protein, rat; D056564:Sirtuin 1