Plasma Leptin Levels in Rat Mother and Offspring during Pregnancy and Lactation

Herrera, Emílio; Lasunción, Miguel A.; Huerta, Lydia Gil; Martín-Hidalgo, Antonia

doi:10.1159/000014286

Cited by 51 publications

(37 citation statements)

References 38 publications

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“…However, leptin levels during the lactating period were not significantly different from the levels found for NP and PW LETO dams. This is according to the previous reports, 38,39 whereas others have reported hypoleptinemia during lactation. 8,12,13 We note that leptin levels of OLETF and LETO NP dams in our present study were in the same range as that reported for 12 weeks postpartum dams.…”

Section: Discussionsupporting

confidence: 89%

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

et al. 2008

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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.

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Section: Discussionsupporting

confidence: 89%

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

et al. 2008

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“…We investigated serum leptin levels in surrogate mothers since leptin has been reported to be transmitted via mother's milk (26) and the administration of leptin to young (up to 6 weeks of age) but not adult female NOD mice has been found to accelerate the development of insulitis with an increased Th1 response and ␥ interferon-mRNA expression (27). In a previous study (26), maternal plasma leptin levels were reported to correlate significantly with those in their respective pups during lactation. In the present study, the serum leptin level was higher in pregnant ICR and DBA/2J surrogate mothers than in the corresponding NOD mice.…”

Section: Discussionmentioning

confidence: 99%

Maternal Factors in a Model of Type 1 Diabetes Differentially Affect the Development of Insulitis and Overt Diabetes in Offspring

et al. 2005

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Type 1 diabetes, a multifactorial disease involving genetic and environmental factors, results from the destruction of pancreatic ␤-cells. The maternal environment has been suggested to be important in the development of diabetes. To assess the role of maternal factors in the development of insulitis and overt diabetes, we transplanted pre-implantation stage embryos of nonobese diabetic (NOD) mice, a model of type 1 diabetes, into the uterus of each recipient. Recipients were ICR and DBA/2J mice without diabetic genetic predisposition and NOD mice not exhibiting overt diabetes during the experiment; offspring were designated as NOD/ICR, NOD/DBA, and NOD/NOD, respectively; unmanipulated NOD offspring were also examined. NOD/ICR and NOD/ DBA offspring developed insulitis significantly earlier than NOD/NOD offspring. However, overt diabetes was significantly suppressed in NOD/ICR and NOD/DBA offspring in comparison with NOD/NOD offspring. Insulin autoantibodies (IAAs) were undetectable in ICR and DBA/2J surrogate mothers and in NOD/ICR and NOD/ DBA offspring at the onset of insulitis, suggesting that maternal factors other than transmitted IAAs induced the earlier onset. The present study indicates that altered maternal factors modify the immune response to islets, which in turn might affect the pathogenic course from insulitis to overt diabetes. Diabetes 54:2026 -2031, 2005 H uman type 1 diabetes is characterized by the establishment of autoimmune insulitis, which precedes ␤-cell destruction, culminating in hypoinsulinemia and hyperglycemia. Human type 1 diabetic patients spontaneously develop a diabetic syndrome that is controlled by both genetic and environmental factors (1,2). The environmental triggers of islet autoimmunity and type 1 diabetes are essentially unknown but are considered likely to operate early in life, possibly even in utero (3). Previous studies have linked the risk of type 1 diabetes to congenital rubella infection, but noncongenital infection does not appear to convey this risk, indicating the importance of pre-or perinatal events as triggers of islet autoimmunity (4 -6). It has been suggested that maternal environment and maternally transmitted insulin autoantibodies (IAAs) in particular modify the risk of the development of autoimmune diabetes in offspring (7); however, it was recently reported (8) that fetal exposure to IAAs did not increase the risk of diabetes development in nonobese diabetic (NOD) mice. The exact role of maternal environmental factors and their relationship in the initiation and modification of the pathogenesis of diabetes in each diabetic individual remain largely unknown. In our previous study (9), by transplanting NOD embryos into the uterus of a recipient ICR mouse, we analyzed genetic predisposition versus diabetic environment and the interaction between these two factors in NOD embryos as causes of congenital malformation.In the present study, using the same experimental strategy, the onset and incidence of insulitis and overt diabetes were examined in offspring ...

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“…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.…”

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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

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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,...

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Plasma Leptin Levels in Rat Mother and Offspring during Pregnancy and Lactation

Cited by 51 publications

References 38 publications

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

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

Maternal Factors in a Model of Type 1 Diabetes Differentially Affect the Development of Insulitis and Overt Diabetes in Offspring

Leptin secretion and hypothalamic neuropeptide and receptor gene expression in sheep

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