Changes in Leptin Levels during Lactation: Implications for Lactational Hyperphagia and Anovulation

Woodside, Barbara; Abizaid, Alfonso; Walker, Claire‐Dominique

doi:10.1006/hbeh.2000.1598

Cited by 73 publications

(75 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We now show that, as in rodents and humans (Kawai et al 1997, Brogan et al 1999, Butte et al 1999, Woodside et al 2000, the transition from pregnancy to lactation in dairy cows is associated with a reduction in the plasma concentration of leptin. This similarity exists despite the use of different strategies by these species to accommodate the energy needs of early lactation.…”

Section: Discussionsupporting

confidence: 60%

“…The role of leptin in regulating complex and dynamic changes in energy balance (EB), such as those taking place during the transition from pregnancy to lactation, has received only limited attention (Kawai et al 1997, Brogan et al 1999, Butte et al 1999, Woodside et al 2000; no information is available in dairy cattle, a species which suffers from a more intense energy deficit after parturition than do humans or rodents (Barber et al 1997, Bauman 2000. As a first step towards understanding the role of leptin in dairy cattle, we have measured changes in the concentration of plasma leptin during the periparturient period.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Decreased concentration of plasma leptin in periparturient dairy cows is caused by negative energy balance

Block

Butler²,

Ehrhardt³

et al. 2001

Journal of Endocrinology

284

229

View full text Add to dashboard Cite

Dairy cows suffer from an intense energy deficit at parturition due to the onset of copious milk synthesis and depressed appetite. Despite this deficit, maternal metabolism is almost completely devoted to the support of mammary metabolism. Evidence from rodents suggests that, during periods of nutritional insufficiency, a reduction in plasma leptin serves to co-ordinate energy metabolism. As an initial step to determine if leptin plays this role in periparturient dairy cows, changes in the plasma concentration of leptin were measured during the period from 35 days before to 56 days after parturition. The plasma concentration of leptin was reduced by 50% after parturition and remained depressed during lactation despite a gradual improvement in energy balance; corresponding changes occurred in the abundance of leptin mRNA in white adipose tissue. To determine whether negative energy balance caused this reduction in circulating leptin, cows were either milked or not milked after parturition. Absence of milk removal eliminated the energy deficit of early lactation, and doubled the plasma concentration of leptin. The plasma concentration of leptin was positively correlated with plasma concentrations of insulin and glucose, and negatively correlated with plasma concentrations of growth hormone and non-esterified fatty acids. In conclusion, the energy deficit of periparturient cows causes a sustained reduction in plasma leptin. This reduction could benefit early lactating dairy cows by promoting a faster increase in feed intake and by diverting energy from non-vital functions such as reproduction.

show abstract

Section: Discussionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Decreased concentration of plasma leptin in periparturient dairy cows is caused by negative energy balance

Block

Butler²,

Ehrhardt³

et al. 2001

Journal of Endocrinology

284

229

View full text Add to dashboard Cite

show abstract

“…However, although the lactating ewes in the study were fed ad libitum, food intake of the control, nonlactating ewes was restricted to maintain a constant body weight over the previous 24 wk (30), which could have decreased their serum leptin concentrations (26,47). Previous studies with rats have also shown that serum leptin is decreased by lactation (16,36,39,56,65,74). However, in the daytime at least, the fall in leptin concentration is much smaller in rats than in sheep.…”

Section: Discussionmentioning

confidence: 99%

“…Key targets are neurons in the hypothalamic arcuate nucleus (ARC) expressing the signaling form of the leptin receptor (OB-Rb); these are the orexigenic peptides neuropeptide Y (NPY) and agouti-related peptide (AGRP) and the anorexigenic peptides proopiomelanocortin (POMC, precursor for melanocortins) and cocaine-and amphetamine-regulated transcript (CART) (4,5,31,62,64,72). Adipose leptin gene expression and serum leptin concentrations are reported to be reduced during lactation in the monogastric rat in most (16,36,39,56,65,74), but not all (17,19,61), studies. NPY (18,21,43,44,54,55,63,71) and AGRP (18) are upregulated, and POMC is downregulated (54,63) in the hypothalamus during lactation in the rat.…”

mentioning

confidence: 99%

Leptin secretion and hypothalamic neuropeptide and receptor gene expression in sheep

Sørensen

Adam²,

Findlay³

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Sheep were fed ad libitum and killed at 6 and 18 days of lactation; ad libitum-fed nonlactating sheep were killed as controls. Despite increased food intake, lactating ewes were in negative energy balance. Lactation decreased plasma leptin and adipose tissue leptin mRNA concentrations. OB-Rb gene expression, determined by in situ hybridization, was increased in the hypothalamic arcuate nucleus (ARC) and ventromedial hypothalamic nucleus (VMH) at both stages of lactation. Neuropeptide Y (NPY) was increased by lactation in both the ARC and dorsomedial hypothalamus (DMH), although increased gene expression in the DMH was only apparent at day 18 of lactation. Gene expression was decreased for cocaine-and amphetamine-regulated transcript (CART) in the ARC and VMH and for proopiomelanocortin in ARC during lactation. Agouti-related peptide gene expression was increased in the ARC, and melanocortin receptor expression was unchanged in both the ARC and VMH with lactation. Thus the hypoleptinemia of lactation may activate NPY orexigenic pathways and attenuate anorexigenic melanocortin and CART pathways in the hypothalamus to promote the hyperphagia of lactation. hypothalamic neuropeptides; appetite NUTRIENT REQUIREMENTS ARE markedly increased during lactation to meet the demands for milk production (7,70). In most mammals, these additional requirements are met primarily by increasing food intake (7,20,70), but factors regulating the hyperphagia of lactation are not well understood. In addition, in many species, the increased intake is insufficient to meet the metabolic demands, resulting in a state of negative energy balance during early lactation when body lipid reserves are mobilized (7,69). In some species such as the rat, the degree of negative energy balance is usually slight, with animals mobilizing ϳ1 g fat/day (7). Domestic ruminants, however, usually exhibit a greater degree of negative energy balance during early lactation (7, 11), which can impact on their welfare and productivity (28), yet the regulatory mechanisms have not been elucidated.It is postulated that leptin, a peptide hormone secreted by adipose tissue (75), could play a role in the hyperphagia of lactation. Leptin acts on hypothalamic neuronal systems to regulate energy balance and neuroendocrine function; in particular, a reduction in circulating leptin is a potent signal of negative energy balance, activating compensatory orexigenic pathways in the hypothalamus (3-5, 35, 64). Key targets are neurons in the hypothalamic arcuate nucleus (ARC) expressing the signaling form of the leptin receptor (OB-Rb); these are the orexigenic peptides neuropeptide Y (NPY) and agouti-related peptide (AGRP) and the anorexigenic peptides proopiomelanocortin (POMC, precursor for melanocortins) and cocaine-and amphetamine-regulated transcript (CART) (4,5,31,62,64,72). Adipose leptin gene expression and serum leptin concentrations are reported to be reduced during lactation in the monogastric rat in most (16,36,39,56,65,74), but not all (17,19,61), studies. NPY (18,21,...

show abstract

“…7 Hyperphagia in lactating female rats is associated with decreased sensitivity to the satiety effects of CCK, 1 and with reduced blood leptin levels relative to nonlactating rats. [8][9][10][11] Although the hypoleptinemia should facilitate the hyperphagia of lactation, other orexigenic signals must also be involved. 12,13 During lactation, the amount of hypothalamic neuropeptide Y (NPY) increases 8 mainly in the DMH.…”

Section: Introductionmentioning

confidence: 99%

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

et al. 2008

View full text Add to dashboard Cite

Objective: To understand the adaptation to lactation of obese rats, by studying the interplay among the gut hormone cholecystokinin (CCK), the adiposity hormone leptin and the affiliation hormone oxytocin in modulating body mass and fat storage. Design: Strain differences were examined between Otsuka Long Evans Tokushima Fatty (OLETF) rats lacking expression of functional CCK-1 receptors and Long Evans Tokushima Otsuka (LETO) controls, tested as nulliparous dams, at the 7 and 15th lactation day, at weaning (lactation day 22) or 8 weeks postweaning. Measurements: We measured body mass, fat pads (brown, retroperitoneal and inguinal) and inguinal adipocytes. Plasma levels of leptin and oxytocin were determined. Results: Fat depots of LETO female rats were larger during lactation compared to the levels found in postweaning and nulliparous female rats. LETO female rats gained weight and accumulated fat during pregnancy and lactation, returning to their normal fat levels postweaning. In contrast, OLETF female rats presented lower body weight and fat depots during the lactation period than nulliparous dams, and regained the weight and fat postweaning. Plasma leptin and oxytocin were highly correlated and followed the same pattern. OLETF leptin levels were highly correlated with fat depot and inguinal cell surface. No significant correlation was found for LETO parameters. Conclusions: Pregnancy and lactation are energy-consuming events, which naturally induce female rats to increase food intake and accumulate fat. When challenged by the demands of rapidly growing preobese OLETF pups, OLETF dams' fat stores are reduced to lean, LETO levels. During lactation, sensitivity of the oxytocinergic neurons descending from the paraventricular nuclei to the nucleus of the solitary tract to CCK is reduced. We theorized that this pathway is not available to OLETF female rats that lack functional CCK-1 receptors to mediate the signal. The current study contributes to the understanding of the female body's adaptation to lactation.

show abstract

Changes in Leptin Levels during Lactation: Implications for Lactational Hyperphagia and Anovulation

Cited by 73 publications

References 55 publications

Decreased concentration of plasma leptin in periparturient dairy cows is caused by negative energy balance

Decreased concentration of plasma leptin in periparturient dairy cows is caused by negative energy balance

Leptin secretion and hypothalamic neuropeptide and receptor gene expression in sheep

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

Contact Info

Product

Resources

About