Leptin Is Present in Human Milk and Is Related to Maternal Plasma Leptin Concentration and Adiposity

Houseknecht, Karen L.; McGuire, Michelle K.; Portocarrero, Carla; McGuire, Mark A.; Beerman, Kathy A.

doi:10.1006/bbrc.1997.7736

Cited by 189 publications

(193 citation statements)

References 23 publications

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“…It has been observed that a postnatal surge in plasma leptin might serve as a key developmental signal (Bouret and Simerly, 2006). Some studies in literature suggest a relationship between leptin levels in BM and serum leptin concentration in lactating mothers, probably because of the ability of leptin to be transferred from serum to BM (Houseknecht et al, 1997;Weyermann et al, 2006), and we recently observed a higher leptin concentration in BF infants than in artificially fed ones (Savino et al, 2005(Savino et al, , 2006.…”

Section: Introductionsupporting

confidence: 56%

Evaluation of leptin in breast milk, lactating mothers and their infants

et al. 2010

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Background/Objectives: Leptin is present in human milk, but it is not clear what the relationship between breast milk (BM) leptin levels and maternal and infant serum leptin concentrations is. The objective of this study was to evaluate the leptin concentration in BM and to investigate its relationship with infants' and mothers' anthropometric parameters and with serum leptin concentration in breast-fed (BF) infants and lactating mothers. Subjects/Methods: We enrolled 36 adequate for gestational age healthy, exclusively BF, term infants aged o6 months. Leptin concentration in serum and BM was determined by radioimmunoassay (RIA) test (human-leptin-RIA-sensitive, Mediagnost). Infants' and mothers' weights, lengths and body mass indexes (BMI) were measured. Results: The median leptin concentration was 3.42 ng/ml (interquartile range (IR): 2.65) in BF infants' serum, 3.02 ng/ml (IR: 2.85) in mothers' serum (n ¼ 17) and 0.51 ng/ml (IR: 0.34) in BM (n ¼ 24). BM leptin concentrations were significantly lower than serum BF infant (Po0.001) and maternal (Po0.001) leptin levels. Infant serum leptin concentration correlated positively with infant weight (r ¼ 0.437, P ¼ 0.008) and BMI (r ¼ 0.561, P ¼ 0.004). Mother serum leptin levels correlated positively with weight (r ¼ 0.755, Po0.001) and BMI (r ¼ 0.661, P ¼ 0.007). No correlations were found between BM leptin and serum leptin concentrations in BF infants and mothers. Conclusions: We confirmed the presence of leptin in BM at a lower concentration than that found in infant and lactating mother serum. We observed a positive correlation between serum leptin levels in BF infants and their growth parameters.

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Section: Introductionsupporting

confidence: 56%

Evaluation of leptin in breast milk, lactating mothers and their infants

et al. 2010

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Section: Discussionmentioning

confidence: 99%

“…18,19 Some authors have found a positive correlation between maternal BMI or adiposity and milk leptin concentration. 19,58 We studied milk leptin concentration during the lactating period in a group of 28 non-obese mothers and also found a wide variation, ranging from values under the detection limit of the assay (o0.0078 ng/ml) to 0.853 ng/ml, with a mean value of 0.156 ng/ml. 59 Considering the amount of leptin supplied to rats in the present study (five times the average amount of the daily leptin intake from the mother's milk), if this could be extrapolated to humans, the amount of leptin to be supplied would be within the range of physiological doses of leptin intake from maternal milk.…”

Section: Discussionmentioning

confidence: 99%

“…4,[8][9][10] Although leptin is mainly produced by the adipose tissue, this hormone is also produced by other tissues, such as stomach, [11][12][13] placenta, 14,15 skeletal muscle 16 and mammary epithelium, 17 and it is naturally present in maternal milk. 18,19 Although leptin produced by the adipose tissue is known to play a main role in the chronic control of energy balance, the role of leptin produced by the stomach has been related with the short-term control of food intake, acting as a satiety signal. 13,20 There is evidence indicating that feeding stimulates the secretion of leptin by the stomach in humans 12,13 and in rats, 11,21 and pepsinogen secretagogues such as cholecystokinin (CCK), gastrin or secretin also induce gastric leptin release in rats.…”

Section: Introductionmentioning

confidence: 99%

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The intake of physiological doses of leptin during lactation in rats prevents obesity in later life

et al. 2007

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Ciber Fisiopatología obesidad y nutrición (CB06/03) Instituto Salud Carlos III, SpainBackground: There is epidemiological evidence that perinatal nutritional factors may have long-term effects on obesity. Which nutrients or food components are involved in this programming mechanism are unknown. Breast milk contains leptin, a hormone that regulates food intake and energy expenditure, and previous studies in rats have shown that leptin orally administered during lactation exerts anorexigenic effects. Objective: To evaluate whether supplementation with physiological doses of oral leptin during lactation has long-term effects on body weight regulation. Design: A daily oral dose of leptin (equivalent to five times the amount of leptin ingested normally from maternal milk during the suckling period) or the vehicle was given to suckling male rats during lactation. Animals were fed after weaning with a normal fat (NF) or a high-fat (HF) diet. We followed body weight and food intake of animals until the age of 6 months, and measured the size of adipose tissue depots, the thermogenic capacity, the expression of leptin in the stomach and adipose tissues and the expression of two appetite-related peptides (neuropeptide Y (NPY) and proopiomelanocortin (POMC)), leptin receptor (OB-Rb) and suppressor of cytokine signalling 3 (SOCS-3) in the hypothalamus at the age of 6 months. Results: Leptin-treated animals had, in adulthood, lower body weight and fat content and ate fewer calories than their untreated controls. Unlike adipocitary leptin production, adult animals that were leptin-treated during lactation displayed higher gastric leptin production without changes in OB-Rb mRNA levels. In addition, in response to HF diet, leptin-treated animals (contrary to controls) showed lower hypothalamic NPY/POMC mRNA ratio. Hypothalamic OB-Rb mRNA levels decreased in control animals as an effect of HF diet feeding, but remained unchanged in leptin-treated animals; SOCS-3 mRNA levels were lower in leptin-treated animals than in their controls, both under normal or HF diet. Conclusion: The animals that received leptin during lactation become more protected against fat accumulation in adult life and seem to be more sensitive to the short-and long-term regulation of food intake by leptin. Thus, leptin plays an important role in the earlier stages of neonatal life, as a component of breast milk, in the prevention of later obesity.

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“…18,19 The clinical relevance of these observations, like the ontogeny of early-life leptin levels in humans, has yet to be established, particularly in the context that leptin is present in breast milk 20 but not in infant formulae, and that breast-feeding has been found to lower the risk for obesity compared with formula feeding. 21,22 Nonetheless, the findings that low leptin levels in cord blood closely reflect low adipose mass at birth, and strongly predict high rates of weight gain during infancy 23 , are consistent with a role for major perturbations in leptin production in developmental programming.…”

Section: Developmental Programming and Thrifty Phenotypesmentioning

confidence: 99%

Thrifty energy metabolism in catch-up growth trajectories to insulin and leptin resistance

Dulloo

2008

Best Practice & Research Clinical Endocrinology & Metab

104

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Catch-up growth early in life (after fetal, neonatal or infantile growth retardation) is a major risk factor for later obesity, type-2 diabetes and cardiovascular diseases. These risks are generally interpreted alongside teleological arguments that environmental exposures which hinder growth early in life lead to programming of 'thrifty mechanisms' that are adaptive during the period of limited nutrient supply (or growth constraint), but which increase risks for diseases during improved nutrition and catch-up growth later in life. This paper addresses this notion of 'thrifty mechanisms' in the light of evidence that catch-up growth is characterized by a disproportionately higher rate of fat gain relative to lean tissue gain, and that such preferential catch-up fat is in part driven by energy conservation mechanisms operating via suppressed thermogenesis. It provides a molecular-physiological framework which integrates emerging insights into mechanisms by which this thrifty 'catch-up fat' phenotype cross-links with insulin and leptin resistance.

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Leptin Is Present in Human Milk and Is Related to Maternal Plasma Leptin Concentration and Adiposity

Cited by 189 publications

References 23 publications

Evaluation of leptin in breast milk, lactating mothers and their infants

Evaluation of leptin in breast milk, lactating mothers and their infants

The intake of physiological doses of leptin during lactation in rats prevents obesity in later life

Thrifty energy metabolism in catch-up growth trajectories to insulin and leptin resistance

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