Leptin as a breast milk component for the prevention of obesity

Palou, Mariona; Picó, Catalina

doi:10.1093/nutrit/nuy046

Cited by 51 publications

(106 citation statements)

References 173 publications

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“…Leptin absorption from colostrum was less clear in previous studies, but an elevated plasma concentration of leptin was also associated with colostrum feeding (Blum et al, 2005;Schäff et al, 2014;Kesser et al, 2017). Absorption of colostral leptin occurs in rats and humans (Szymeczko et al, 2009;Woliński et al, 2014;Palou et al, 2018). Previous studies indicated lower leptin and adiponectin concentrations in milk or milk-based formulas than in colostrum (Kesser et al, 2015(Kesser et al, , 2017.…”

Section: Discussionmentioning

confidence: 94%

“…The question remains whether the absorbed leptin and adiponectin are of physiological relevance in neonatal calves. Both hormones are known for their improvement of insulin sensitivity (Havel, 2002;Yamauchi and Kadowaki, 2013;Palou et al, 2018). Interestingly, insulin concentrations in blood plasma on the first day of life were much greater after formula feeding than after colostrum feeding, whereas the plasma glucose concentration was similar between the feeding groups.…”

Section: Discussionmentioning

confidence: 98%

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Effects of colostrum instead of formula feeding for the first 2 days postnatum on whole-body energy metabolism and its endocrine control in neonatal calves

Liermann

Schäff

Gruse

et al. 2020

Journal of Dairy Science

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Colostrum provides high amounts of nutritive and non-nutritive substrates, which are essential for calf nutrition and passive immunization. Colostral growth factors and hormones have beneficial effects on postnatal maturation and may affect substrate utilization and energy expenditure in neonatal calves. We tested the hypothesis that energy metabolism and its endocrine regulation differ during the first 10 d of life in calves fed either colostrum or a milk-based formula with a similar nutrient composition to colostrum, but largely depleted of bioactive substances, for the first 2 d postnatum. Male Holstein calves (n = 18) were fed either pooled colostrum (COL; n = 9) or a milk-based formula (FOR; n = 9) for the first 2 d of life. From d 3 on, all calves received same milk replacer. On d 2 and 7 of life, calves were placed in a respiration chamber for indirect calorimetric measurements to calculate heat production, fat (FOX) and carbohydrate oxidation (COX), as well as respiratory quotient. Blood was sampled on d 1 before first colostrum intake and on d 2, 3, 7, 8, 9, and 10 before morning feeding, to measure plasma concentrations of immunoglobulins, metabolites, and hormones. Additional postprandial blood samples were taken on d 1 and 9 at 30, 60, 120, 240, and 420 min after milk feeding. Liver samples were collected on d 10 of life to determine gene expression related to energy metabolism. Formula-fed calves showed lower plasma concentrations of total protein, immunoglobulins, haptoglobin, leptin, adiponectin, and insulin-like growth factor (IGF) binding protein (IGFBP)-4 during the whole study but temporarily higher plasma concentrations of urea, insulin, glucagon, triglyceride, and cholesterol on the first day after feeding, compared with concentrations in COL. The temporary increase in glucagon, triglyceride, and cholesterol on d 1 reversed on d 2 or 3, showing higher concentrations in COL than in FOR calves. In FOR, IGF-I, IGFBP-2, and IGFBP-3 were lower on d 3 than in COL. Interestingly, FOR calves had higher heat production during respiratory measurements on d 2 and higher body temperature on d 2, 3, and 5 than those of COL. The hepatic mRNA abundance of cytosolic phosphoenolpyruvate carboxykinase was higher in FOR than in COL. Our results indicate that first milk feeding after birth influenced whole-body energy expenditure but not FOX and COX in neonatal calves, and the absorption of colostral leptin and adiponectin might affect insulin sensitivity on d 1 of life.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 98%

Effects of colostrum instead of formula feeding for the first 2 days postnatum on whole-body energy metabolism and its endocrine control in neonatal calves

Liermann

Schäff

Gruse

et al. 2020

Journal of Dairy Science

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“…These metabolic hormones play important roles by potentiating neuroendocrine signalling and tissue maturation and by establishing a healthy function of energy metabolism in critical stages of life development. 37,38 As elegantly demonstrated, intracerebroventricular leptin exposure in the embryonic brain permanently programmed reduced cholinergic innervation of pancreatic β-cells, as well as long-term impairment in glucose homeostasis. 39 Interestingly, the authors showed an embryonic inhibitory effect of leptin on the growth of cholinergic neurites in the hindbrain that influences parasympathetic signalling upon the endocrine function of the pancreas 39 ; in our study, we found low parasympathetic tonus associated with hypoleptinaemia.…”

Section: Discussionmentioning

confidence: 99%

Cholinergic-pathway-weakness-associated pancreatic islet dysfunction: a low-protein-diet imprint effect on weaned rat offspring

Mathias

Miranda

Barella

et al. 2020

J Dev Orig Health Dis

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Currently, metabolic disorders are one of the major health problems worldwide, which have been shown to be related to perinatal nutritional insults, and the autonomic nervous system and endocrine pancreas are pivotal targets of the malprogramming of metabolic function. We aimed to assess glucose–insulin homeostasis and the involvement of cholinergic responsiveness (vagus nerve activity and insulinotropic muscarinic response) in pancreatic islet capacity to secrete insulin in weaned rat offspring whose mothers were undernourished in the first 2 weeks of the suckling phase. At delivery, dams were fed a low-protein (4% protein, LP group) or a normal-protein diet (20.5% protein, NP group) during the first 2 weeks of the suckling period. Litter size was adjusted to six pups per mother, and rats were weaned at 21 days old. Weaned LP rats presented a lean phenotype (P < 0.01); hypoglycaemia, hypoinsulinaemia and hypoleptinaemia (P < 0.05); and normal corticosteronaemia (P > 0.05). In addition, milk insulin levels in mothers of the LP rats were twofold higher than those of mothers of the NP rats (P < 0.001). Regarding glucose–insulin homeostasis, weaned LP rats were glucose-intolerant (P < 0.01) and displayed impaired pancreatic islet insulinotropic function (P < 0.05). The M3 subtype of the muscarinic acetylcholine receptor (M3mAChR) from weaned LP rats was less responsive, and the superior vagus nerve electrical activity was reduced by 30% (P < 0.01). A low-protein diet in the suckling period malprogrammes the vagus nerve to low tonus and impairs muscarinic response in the pancreatic β-cells of weaned rats, which are imprinted to secrete inadequate insulin amounts from an early age.

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“…Even though, according to World Health Organization, all infants should be exclusively breastfed from birth up to 6 months of age, most countries are still not doing enough to support mothers despite the potential health benefits as well as positive economic implications (Prell & Koletzko, ; Walters, Phan, & Mathisen, ). Breastfeeding is crucial to establish optimal or reference intake values for leptin during lactation, thereby designing personalized patterns of nutrition achieved through postnatal programming of a healthy phenotype in early childhood that will remain into adulthood (Palou, Pico, & Palou, ).…”

Section: Future Considerationsmentioning

confidence: 99%

“…Breastfeeding is crucial to establish optimal or reference intake values for leptin during lactation, thereby designing personalized patterns of nutrition achieved through postnatal programming of a healthy phenotype in early childhood that will remain into adulthood (Palou, Pico, & Palou, 2018).…”

Section: Future Cons Ider Ationsmentioning

confidence: 99%

Diet‐induced DNA methylation within the hypothalamic arcuate nucleus and dysregulated leptin and insulin signaling in the pathophysiology of obesity

Samodien

Erasmus

Mabasa

et al. 2019

Food Science & Nutrition

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Obesity rates continue to rise in an unprecedented manner in what could be the most rapid population‐scale shift in human phenotype ever to occur. Increased consumption of unhealthy, calorie‐dense foods, coupled with sedentary lifestyles, is the main factor contributing to a positive energy balance and the development of obesity. Leptin and insulin are key hormones implicated in pathogenesis of this disorder and are crucial for controlling whole‐body energy homeostasis. Their respective function is mediated by the counterbalance of anorexigenic and orexigenic neurons located within the hypothalamic arcuate nucleus. Dysregulation of leptin and insulin signaling pathways within this brain region may contribute not only to the development of obesity, but also systemically affect the peripheral organs, thereby manifesting as metabolic diseases. Although the exact mechanisms detailing how these hypothalamic nuclei contribute to disease pathology are still unclear, increasing evidence suggests that altered DNA methylation may be involved. This review evaluates animal studies that have demonstrated diet‐induced DNA methylation changes in genes that regulate energy homeostasis within the arcuate nucleus, and elucidates possible mechanisms causing hypothalamic leptin and insulin resistance leading to the development of obesity and metabolic diseases.

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Leptin as a breast milk component for the prevention of obesity

Cited by 51 publications

References 173 publications

Effects of colostrum instead of formula feeding for the first 2 days postnatum on whole-body energy metabolism and its endocrine control in neonatal calves

Effects of colostrum instead of formula feeding for the first 2 days postnatum on whole-body energy metabolism and its endocrine control in neonatal calves

Cholinergic-pathway-weakness-associated pancreatic islet dysfunction: a low-protein-diet imprint effect on weaned rat offspring

Diet‐induced DNA methylation within the hypothalamic arcuate nucleus and dysregulated leptin and insulin signaling in the pathophysiology of obesity

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