Effects of leptin infusion during peak lactation on food intake, body composition, litter growth, and maternal neuroendocrine status in female Brandt's voles (Lasiopodomys brandtii).
During lactation, female small mammals frequently reduce their fat reserves to very low levels. The function of this reduction is unclear, as calculations suggest that the contribution of the withdrawn energy from fat to the total energy balance of lactation is trivial. An alternative hypothesis is that reducing fat leads to a reduction in circulating adipokines, such as leptin, that play a role in stimulating the hyperphagia of lactation. We investigated the role of circulating leptin in lactation by repleting leptin levels using miniosmotic pumps during the last 7 days of lactation in Brandt's voles (Lasiopodomys brandtii), a model small wild mammal we have extensively studied in the context of lactation energy demands. Repletion of leptin resulted in a dose-dependent reduction of body mass and food intake in lactating voles. Comparisons to nonreproducing individuals suggests that the reduced leptin in lactation, due to reduced fat stores, may account for ∼16% of the lactational hyperphagia. Reduced leptin in lactation may, in part, cause lactational hyperphagia via stimulatory effects on hypothalamic orexigenic neuropeptides (neuropeptide Y and agouti-related peptide) and inhibition of the anorexigenic neuropeptide (proopiomelanocortin). These effects were reversed by the experimental repletion of leptin. There was no significant effect of leptin treatment on daily energy expenditure, milk production or pup growth, but leptin repletion did result in a reversal of the suppression of uncoupling protein-1 levels in brown adipose tissue, indicating an additional role for reducing body fat and leptin during peak lacation.
Institute of Zoology, Chinese Academy of Sciences, Benchen Xilu, Chaoyang, Beijing 100101, China.
Jian-Guo
JG
Cui
Gang-Bin
GB
Tang
De-Hua
DH
Wang
John R
JR
Speakman
D000273:Adipose Tissue / Q000187:drug effects; D002001:Adipose Tissue, Brown / Q000187:drug effects / Q000378:metabolism; D054369:Agouti-Related Protein / Q000235:genetics; D000825:Animal Structures / Q000033:anatomy & histology / Q000187:drug effects; D000818:Animals; D000833:Animals, Suckling / Q000254:growth & development*; D003411:Arvicolinae; D001823:Body Composition / Q000187:drug effects* / Q000502:physiology; D001835:Body Weight / Q000187:drug effects; D004435:Eating / Q000187:drug effects* / Q000502:physiology; D002149:Energy Intake / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism; D007774:Lactation / Q000187:drug effects / Q000502:physiology*; D020738:Leptin / Q000008:administration & dosage / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology*; D008099:Liver / Q000033:anatomy & histology / Q000187:drug effects; D024101:Mitochondrial Proteins / Q000378:metabolism; D009478:Neuropeptide Y / Q000235:genetics; D009490:Neurosecretory Systems / Q000187:drug effects* / Q000502:physiology; D009929:Organ Size / Q000187:drug effects; D011333:Pro-Opiomelanocortin / Q000235:genetics; D000071256:Uncoupling Protein 1
D054369:Agouti-Related Protein; D007473:Ion Channels; D020738:Leptin; D024101:Mitochondrial Proteins; D009478:Neuropeptide Y; D000071256:Uncoupling Protein 1; D011333:Pro-Opiomelanocortin