Neonatal overnutrition programming impairs cholecystokinin effects in adultmale rats

Enes-Marques, Silvia; Rojas, Viviana Carolina Trujillo; Batista, Tatiane Helena; Vitor-Vieira, Fernando; Novais, Cíntia O. de; Rafacho, Alex; Giusti‐Paiva, Alexandre

doi:10.1016/j.jnutbio.2020.108494

Cited by 10 publications

(4 citation statements)

References 48 publications

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“…The litter size reduction method programs overweight in adulthood according to several data ( Plagemann et al, 1992 ; Boullu-Ciocca et al, 2005 ; Rodrigues et al, 2009 ; Conceição et al, 2011 ; Ferretti et al, 2011 ; Rodrigues et al, 2011 ). The increased body weight, adiposity and the impairment of lipidic profile in SL animals corroborates with the literature, where animals reared in small litters present obesity-related changes that persist until adulthood, as higher body weight, accompanied by higher FFA ( Bei et al, 2015 ) and total cholesterol, as well as fat depots ( Hahn, 1984 ; Enes-Marques et al, 2020 ), without changes in plasma TG ( Rodrigues et al, 2007 ; Conceição et al, 2013 ).…”

Section: Discussionsupporting

confidence: 90%

Glucocorticoids contribute to metabolic and liver impairments induced by lactation overnutrition in male adult rats

et al. 2023

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Introduction: Lactation overnutrition is a programming agent of energy metabolism, and litter size reduction leads to the early development of obesity, which persists until adulthood. Liver metabolism is disrupted by obesity, and increased levels of circulating glucocorticoids are pointed as a possible mediator for the obesity development, since bilateral adrenalectomy (ADX) can reduce obesity in different models of obesity.Methods: This study aimed to evaluate the effects of glucocorticoids on metabolic changes and liver lipogenesis and insulin pathway induced by lactation overnutrition. For this, on the postnatal day 3 (PND), 3 pups (small litter—SL) or 10 pups (normal litter—NL) were kept with each dam. On PND 60, male Wistar rats underwent bilateral adrenalectomy (ADX) or fictitious surgery (sham), and half of ADX animals received corticosterone (CORT- 25 mg/L) diluted in the drinking fluid. On PND 74, the animals were euthanized by decapitation for trunk blood collection, and liver dissection and storage.Results and Discussion: SL rats presented increased corticosterone, free fatty acids, total and LDL-cholesterol plasma levels, without changes in triglycerides (TG) and HDL-cholesterol. The SL group also showed increased content of liver TG, and expression of fatty acid synthase (FASN), but decreased expression of PI3Kp110 in the liver, compared to NL rats. In the SL group, the ADX decreased plasma levels of corticosterone, FFA, TG and HDL cholesterol, liver TG, and liver expression of FASN, and IRS2, compared to sham animals. In SL animals, CORT treatment increased plasma levels of TG and HDL cholesterol, liver TG, and expression of FASN, IRS1, and IRS2, compared with the ADX group. In summary, the ADX attenuated plasma and liver changes observed after lactation overnutrition, and CORT treatment could reverse most ADX-induced effects. Thus, increased circulating glucocorticoids are likely to play a pivotal role in liver and plasma impairments induced by lactation overnutrition in male rats.

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Section: Discussionsupporting

confidence: 90%

Glucocorticoids contribute to metabolic and liver impairments induced by lactation overnutrition in male adult rats

et al. 2023

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“…Many studies have reported that overnutrition during lactation in rodents not only results in several metabolic disorders but also in cardiovascular alterations that include cardiac dysfunction and the development of hypertension [24][25][26]. The metabolic changes associated with postnatal overfeeding have been widely described [27] and are due to alterations both in the central systems involved in food intake regulation [28][29][30][31] and in peripheral tissues involved in metabolism such as the gastrointestinal system, the liver, and the adipose tissue [32,33]. In this regard, our results agree with previous studies, which have reported that early overnutrition is associated with increased body weight at weaning, which is maintained in adulthood [22,34,35].…”

Section: Discussionmentioning

confidence: 99%

Postnatal Overfeeding during Lactation Induces Endothelial Dysfunction and Cardiac Insulin Resistance in Adult Rats

Tejera-Muñoz,

Guerra-Menéndez,

Amor

et al. 2023

IJMS

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Early overnutrition is associated with cardiometabolic alterations in adulthood, likely attributed to reduced insulin sensitivity due to its crucial role in the cardiovascular system. This study aimed to assess the long-term effects of early overnutrition on the development of cardiovascular insulin resistance. An experimental childhood obesity model was established using male Sprague Dawley rats. Rats were organized into litters of 12 pups/mother (L12-Controls) or 3 pups/mother (L3-Overfed) at birth. After weaning, animals from L12 and L3 were housed three per cage and provided ad libitum access to food for 6 months. L3 rats exhibited elevated body weight, along with increased visceral, subcutaneous, and perivascular fat accumulation. However, heart weight at sacrifice was reduced in L3 rats. Furthermore, L3 rats displayed elevated serum levels of glucose, leptin, adiponectin, total lipids, and triglycerides compared to control rats. In the myocardium, overfed rats showed decreased IL-10 mRNA levels and alterations in contractility and heart rate in response to insulin. Similarly, aortic tissue exhibited modified gene expression of TNFα, iNOS, and IL-6. Additionally, L3 aortas exhibited endothelial dysfunction in response to acetylcholine, although insulin-induced relaxation remained unchanged compared to controls. At the molecular level, L3 rats displayed reduced Akt phosphorylation in response to insulin, both in myocardial and aortic tissues, whereas MAPK phosphorylation was elevated solely in the myocardium. Overfeeding during lactation in rats induces endothelial dysfunction and cardiac insulin resistance in adulthood, potentially contributing to the cardiovascular alterations observed in this experimental model.

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“…In the ARH, CCK expression was decreased during the course of lactation in rats [ 25 ], which could explain the hyperphagia accompanying this period. Furthermore, neonatal overnutrition induced a CCK-resistant phenotype in the offspring [ 67 ], while maternal malnutrition has been shown to reduce CCK levels in the offspring hypothalamus [ 68 ], which may contribute to overweight and metabolic dysfunctions.…”

Section: Discussionmentioning

confidence: 99%

Gut-derived peptide hormone receptor expression in the developing mouse hypothalamus

Cantacorps,

Coull,

Falck

et al. 2023

PLoS ONE

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Objective In adult organisms, a number of receptors have been identified which modulate metabolic processes related to peptides derived from the intestinal tract. These receptors play significant roles in glucose homeostasis, food intake and energy balance. Here we assess these classical metabolic receptors and their expression as well as their potential role in early development of hypothalamic neuronal circuits. Methods Chow-fed C57BL6/N female mice were mated and hypothalamic tissue was collected from offspring across postnatal development (postnatal day 7–21). Subsequent qPCR and Western Blot analyses were used to determine mRNA and protein changes in gut-derived peptide hormone receptors. Correlations to body weight, blood glucose and circulating leptin levels were analyzed. Results We describe the gene expression and dynamic protein regulation of key gut-derived peptide hormone receptors in the early postnatal period of the mouse brain. Specifically, we show changes to Gastric inhibitory polypeptide receptor (GIPR), glucagon-like peptide 1 receptor (GLP1R), and cholecystokinin receptor 2 (CCK2R) in the developing hypothalamus. The changes to GIPR and InsR seem to be strongly negatively correlated with body weight. Conclusions This comprehensive analysis underscores the need to understand the roles of maternal-derived circulating gut hormones and their direct effect on offspring brain development.

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Neonatal overnutrition programming impairs cholecystokinin effects in adultmale rats

Cited by 10 publications

References 48 publications

Glucocorticoids contribute to metabolic and liver impairments induced by lactation overnutrition in male adult rats

Glucocorticoids contribute to metabolic and liver impairments induced by lactation overnutrition in male adult rats

Postnatal Overfeeding during Lactation Induces Endothelial Dysfunction and Cardiac Insulin Resistance in Adult Rats

Gut-derived peptide hormone receptor expression in the developing mouse hypothalamus

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