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Journal articles on the topic 'Postnatal overfeeding'

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Published: 20 April 2024

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1

Sousa, Diana, Mariana Rocha, Andreia Amaro, Marcos Divino Ferreira-Junior, Keilah Valéria Naves Cavalcante, Tamaeh Monteiro-Alfredo, Cátia Barra, et al. "Exposure to Obesogenic Environments during Perinatal Development Modulates Offspring Energy Balance Pathways in Adipose Tissue and Liver of Rodent Models." Nutrients 15, no. 5 (March 4, 2023): 1281. http://dx.doi.org/10.3390/nu15051281.

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Obesogenic environments such as Westernized diets, overnutrition, and exposure to glycation during gestation and lactation can alter peripheral neuroendocrine factors in offspring, predisposing for metabolic diseases in adulthood. Thus, we hypothesized that exposure to obesogenic environments during the perinatal period reprograms offspring energy balance mechanisms. Four rat obesogenic models were studied: maternal diet-induced obesity (DIO); early-life obesity induced by postnatal overfeeding; maternal glycation; and postnatal overfeeding combined with maternal glycation. Metabolic parameters, energy expenditure, and storage pathways in visceral adipose tissue (VAT) and the liver were analyzed. Maternal DIO increased VAT lipogenic [NPY receptor-1 (NPY1R), NPY receptor-2 (NPY2R), and ghrelin receptor], but also lipolytic/catabolic mechanisms [dopamine-1 receptor (D1R) and p-AMP-activated protein kinase (AMPK)] in male offspring, while reducing NPY1R in females. Postnatally overfed male animals only exhibited higher NPY2R levels in VAT, while females also presented NPY1R and NPY2R downregulation. Maternal glycation reduces VAT expandability by decreasing NPY2R in overfed animals. Regarding the liver, D1R was decreased in all obesogenic models, while overfeeding induced fat accumulation in both sexes and glycation the inflammatory infiltration. The VAT response to maternal DIO and overfeeding showed a sexual dysmorphism, and exposure to glycotoxins led to a thin-outside-fat-inside phenotype in overfeeding conditions and impaired energy balance, increasing the metabolic risk in adulthood.

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2

You, Su, Franziska Götz, W. Rohde, and G. Dörner. "Early Postnatal Overfeeding and Diabetes Susceptibility." Experimental and Clinical Endocrinology & Diabetes 96, no. 06 (July 16, 2009): 301–6. http://dx.doi.org/10.1055/s-0029-1211023.

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3

Castellano, Juan M., Agnete H. Bentsen, Miguel A. Sánchez-Garrido, Francisco Ruiz-Pino, Magdalena Romero, David Garcia-Galiano, Enrique Aguilar, et al. "Early Metabolic Programming of Puberty Onset: Impact of Changes in Postnatal Feeding and Rearing Conditions on the Timing of Puberty and Development of the Hypothalamic Kisspeptin System." Endocrinology 152, no. 9 (June 28, 2011): 3396–408. http://dx.doi.org/10.1210/en.2010-1415.

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Kiss1 neurons have recently emerged as a putative conduit for the metabolic gating of reproduction, with leptin being a regulator of hypothalamic Kiss1 expression. Early perturbations of the nutritional status are known to predispose to different metabolic disorders later in life and to alter the timing of puberty; however, the potential underlying mechanisms remain poorly defined. Here we report how changes in the pattern of postnatal feeding affect the onset of puberty and evaluate key hormonal and neuropeptide [Kiss1/kisspeptin (Kp)] alterations linked to these early nutritional manipulations. Female rats were raised in litters of different sizes: small (four pups per dam: overfeeding), normal (12 pups per dam), and large litters (20 pups per litter: underfeeding). Postnatal overfeeding resulted in persistently increased body weight and earlier age of vaginal opening, as an external sign of puberty, together with higher levels of leptin and hypothalamic Kiss1 mRNA. Conversely, postnatal underfeeding caused a persistent reduction in body weight, lower ovarian and uterus weights, and delayed vaginal opening, changes that were paralleled by a decrease in leptin and Kiss1 mRNA levels. Kisspeptin-52 immunoreactivity (Kp-IR) in the hypothalamus displayed similar patterns, with lower numbers of Kp-IR neurons in the arcuate nucleus of postnatally underfed animals, and a trend for increased Kp-positive fibers in the periventricular area of early overfed rats. Yet, gonadotropin responses to Kp at puberty were similar in all groups, except for enhanced responsiveness to low doses of Kp-10 in postnatally underfed rats. In conclusion, our data document that the timing of puberty is sensitive to both overfeeding and subnutrition during early (postnatal) periods and suggest that alterations in hypothalamic expression of Kiss1/kisspeptin may underlie at least part of such programming phenomenon.

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4

Mićić, Bojana, Ana Djordjevic, Nataša Veličković, Sanja Kovačević, Teodora Martić, Djuro Macut, and Danijela Vojnović Milutinović. "AMPK Activation as a Protective Mechanism to Restrain Oxidative Stress in the Insulin-Resistant State in Skeletal Muscle of Rat Model of PCOS Subjected to Postnatal Overfeeding." Biomedicines 11, no. 6 (May 30, 2023): 1586. http://dx.doi.org/10.3390/biomedicines11061586.

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Polycystic ovary syndrome (PCOS) is a common endocrinopathy in women of reproductive age, often associated with obesity and insulin resistance. Childhood obesity is an important predisposing factor for the development of PCOS later in life. Being particularly interested in the interplay between prepubertal obesity and hyperandrogenemia, we investigated the effects of early postnatal overfeeding, accomplished by reducing litter size during the period of suckling, on energy sensing and insulin signaling pathways in the gastrocnemius muscle of a rat model of PCOS-induced by 5α-dihydrotestosterone (DHT). The combination of overfeeding and DHT treatment caused hyperinsulinemia and decreased systemic insulin sensitivity. Early postnatal overfeeding induced defects at critical nodes of the insulin signaling pathway in skeletal muscle, which was associated with reduced glucose uptake in the presence of hyperandrogenemia. In this setting, under a combination of overfeeding and DHT treatment, skeletal muscle switched to mitochondrial β-oxidation of fatty acids, resulting in oxidative stress and inflammation that stimulated AMP-activated protein kinase (AMPK) activity and its downstream targets involved in mitochondrial biogenesis and antioxidant protection. Overall, a combination of overfeeding and hyperandrogenemia resulted in a prooxidative and insulin-resistant state in skeletal muscle. This was accompanied by the activation of AMPK, which could represent a potential therapeutic target in insulin-resistant PCOS patients.

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5

Kappeler, Laurent, Carlos De Magalhaes Filho, Patricia Leneuve, Jie Xu, Nadège Brunel, Christos Chatziantoniou, Yves Le Bouc, and Martin Holzenberger. "Early Postnatal Nutrition Determines Somatotropic Function in Mice." Endocrinology 150, no. 1 (September 18, 2008): 314–23. http://dx.doi.org/10.1210/en.2008-0981.

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Increasing evidence suggests a developmental origin for a number of human diseases, notably after intrauterine or postnatal nutrient deprivation. Nutritional changes readily translate into alterations of somatic growth. However, whereas intrauterine growth retardation often shows postnatal catch-up growth, recovery from food restriction immediately after birth is limited. Therefore, we investigated whether early postnatal nutrition (undernutrition and overfeeding) modifies plasticity of growth through developmental control of the somatotropic hormone axis. We used cross-fostering in mice to induce changes in early nutrition, and examined endocrine growth regulation and the development of specific disease phenotypes in adults. We showed that underfeeding during the early postnatal period delayed growth, whereas overfeeding accelerated it. In both cases, final body size was permanently altered. We found coordinated alterations in pituitary GH, plasma IGF-I and acid labile subunit, and gene expression of hypothalamic GHRH during postnatal development. These changes were consistent with the observed phenotypes. Alterations in the somatotropic axis persisted throughout adulthood. Although limited to the early postnatal period, both underfeeding and overfeeding led to reduced glucose tolerance later in life. These metabolic abnormalities were in line with defective insulin secretion in restricted mice and insulin resistance in overfed mice. Moreover, both restricted and overfed mice had increased arterial blood pressure, suggestive of vascular impairment. Our findings indicate a significant link between early postnatal diet, somatotropic development, and specific late onset diseases in mice. We suggest that, together with other hormones like leptin, IGF-I may play a role in modulating hypothalamic stimulation of the developing somatotropic function. Early postnatal nutrition determines adult activity of the GH axis through an early modulation of hypothalamic GHRH stimulation, probably via hormones like leptin or IGF-I.

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6

Josse, Marie, Eve Rigal, Nathalie Rosenblatt-Velin, Francesca Rochais, Geoffrey Dogon, Luc Rochette, Marianne Zeller, and Catherine Vergely. "Influence of postnatal overfeeding on postnatal heart development in juvenile mice." Archives of Cardiovascular Diseases Supplements 15, no. 2 (May 2023): 192. http://dx.doi.org/10.1016/j.acvdsp.2023.03.029.

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7

Du, Susu, Xiaolei Zhu, Nan Zhou, Wen Zheng, Wei Zhou, and Xiaonan Li. "Curcumin alleviates hepatic steatosis by improving mitochondrial function in postnatal overfed rats and fatty L02 cells through the SIRT3 pathway." Food & Function 13, no. 4 (2022): 2155–71. http://dx.doi.org/10.1039/d1fo03752h.

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Postnatal overfeeding damaged mitochondrial biogenesis and antioxidant response, and increased hepatic lipids and the severity of high-fat-induced NAFLD, while curcumin alleviated hepatic steatosis, at least partially, by enhancing mitochondrial function through SIRT3.

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8

Mićić, Bojana, Ana Teofilović, Ana Djordjevic, Nataša Veličković, Djuro Macut, and Danijela Vojnović Milutinović. "AMPK Activation Is Important for the Preservation of Insulin Sensitivity in Visceral, but Not in Subcutaneous Adipose Tissue of Postnatally Overfed Rat Model of Polycystic Ovary Syndrome." International Journal of Molecular Sciences 23, no. 16 (August 11, 2022): 8942. http://dx.doi.org/10.3390/ijms23168942.

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Polycystic ovary syndrome (PCOS) is a well-known reproductive syndrome usually associated with obesity, insulin resistance, and hyperinsulinemia. Although the first signs of PCOS begin early in adolescence, it is underexplored whether peripubertal obesity predisposes women to PCOS metabolic disturbances. To highlight that, we examined the impact of postnatal overfeeding-induced obesity, achieved by litter size reduction during the suckling period, on metabolic disturbances associated with visceral and subcutaneous adipose tissue (VAT and SAT) function in the 5α-dihydrotestosterone (5α-DHT)-induced animal model of PCOS. We analyzed markers of insulin signaling, lipid metabolism, and energy sensing in the VAT and SAT. Our results showed that postnatally overfed DHT-treated Wistar rats had increased VAT mass with hypertrophic adipocytes, together with hyperinsulinemia and increased HOMA index. In the VAT of these animals, insulin signaling remained unchanged while lipogenic markers decreased, which was accompanied by increased AMPK activation. In the SAT of the same animals, markers of lipogenesis and lipolysis increased, while the activity of AMPK decreased. Taken together, obtained results showed that postnatal overfeeding predisposes development of PCOS systemic insulin resistance, most likely as a result of worsened metabolic function of SAT, while VAT preserved its tissue insulin sensitivity through increased activity of AMPK.

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9

Boubred, Farid, Laurent Daniel, Christophe Buffat, Jean-Marc Feuerstein, Michel Tsimaratos, Charles Oliver, Françoise Dignat-George, Martine Lelièvre-Pégorier, and Umberto Simeoni. "Early postnatal overfeeding induces early chronic renal dysfunction in adult male rats." American Journal of Physiology-Renal Physiology 297, no. 4 (October 2009): F943—F951. http://dx.doi.org/10.1152/ajprenal.90704.2008.

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Low birth weight is associated with an increased risk of hypertension and renal dysfunction at adulthood. Such an association has been shown to involve a reduction of nephron endowment and to be enhanced by accelerated postnatal growth in humans. However, while low-birth-weight infants often undergo catch-up growth, little is known about the long-term vascular and renal effects of accelerated postnatal growth. We surimposed early postnatal overfeeding (OF; reduction of litter size during the suckling period) to appropriate-birth-weight (NBW+OF) and intrauterine growth restriction (IUGR; IUGR+OF) pups, obtained after a maternal gestational low-protein diet. Blood pressure (systolic blood pressure; SBP) and renal function (glomerular filtration rate; GFR) were measured in young and aging offspring. Glomerulosclerosis and nephron number were determined in aging offspring (22 mo). Nephron number was reduced in both IUGR and IUGR+OF male offspring (by 24 and 26%). GFR was reduced by 40% in 12-mo-old IUGR+OF male offspring, and both NBW+OF and IUGR+OF aging male offspring had sustained hypertension (+25 mmHg) and glomerulosclerosis, while SBP and renal function were unaffected in IUGR aging offspring. Female offspring were unaffected. In conclusion, in this experimental model, early postnatal OF in the neonatal period has major long-lasting effects. Such effects are gender dependent. Reduced nephron number alone, associated with IUGR, may not be sufficient to induce long-lasting physiological alterations, and early postnatal OF acts as a “second hit.” Early postnatal OF is a suitable model with which to study the long-term effects of postnatal growth in the pathogenesis of vascular disorders and renal disease.

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10

Josse, Marie, Eve Rigal, Nathalie Rosenblatt-Velin, Luc Rochette, Marianne Zeller, Charles Guenancia, and Catherine Vergely. "Programming of Cardiovascular Dysfunction by Postnatal Overfeeding in Rodents." International Journal of Molecular Sciences 21, no. 24 (December 11, 2020): 9427. http://dx.doi.org/10.3390/ijms21249427.

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Nutritional environment in the perinatal period has a great influence on health and diseases in adulthood. In rodents, litter size reduction reproduces the effects of postnatal overnutrition in infants and reveals that postnatal overfeeding (PNOF) not only permanently increases body weight but also affects the cardiovascular function in the short- and long-term. In addition to increased adiposity, the metabolic status of PNOF rodents is altered, with increased plasma insulin and leptin levels, associated with resistance to these hormones, changed profiles and levels of circulating lipids. PNOF animals present elevated arterial blood pressure with altered vascular responsiveness to vasoactive substances. The hearts of overfed rodents exhibit hypertrophy and elevated collagen content. PNOF also induces a disturbance of cardiac mitochondrial respiration and produces an imbalance between oxidants and antioxidants. A modification of the expression of crucial genes and epigenetic alterations is reported in hearts of PNOF animals. In vivo, a decreased ventricular contractile function is observed during adulthood in PNOF hearts. All these alterations ultimately lead to an increased sensitivity to cardiac pathologic challenges such as ischemia-reperfusion injury. Nevertheless, caloric restriction and physical exercise were shown to improve PNOF-induced cardiac dysfunction and metabolic abnormalities, drawing a path to the potential therapeutic correction of early nutritional programming.

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11

Habbout, Ahmed. "247 Metabolic and cardiovascular consequences of postnatal overfeeding in mice." Archives of Cardiovascular Diseases Supplements 3, no. 1 (January 2011): 81. http://dx.doi.org/10.1016/s1878-6480(11)70249-x.

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12

Rigal, E., C. Greco, A. Méloux, C. Yzydorczyk, L. Rochette, U. Simeoni, and C. Vergely-Vandriesse. "Long-term impact of postnatal overfeeding on myocardial protective pathways." Archives of Cardiovascular Diseases Supplements 10, no. 2 (April 2018): 188–89. http://dx.doi.org/10.1016/j.acvdsp.2018.02.031.

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13

Habbout, Ahmed, Stéphanie Delemasure-Chalumeau, Carole Richard, Luc Rochette, and Catherine Vergely. "Metabolic, Oxidative and Cardiovascular Consequences of Postnatal Overfeeding in Mice." Free Radical Biology and Medicine 49 (January 2010): S42. http://dx.doi.org/10.1016/j.freeradbiomed.2010.10.090.

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14

MohanKumar, S. M. J., T. D. Rajendran, A. K. Vyas, V. Hoang, N. Asirvatham-Jeyaraj, A. Veiga-Lopez, N. B. Olivier, V. Padmanabhan, and P. S. MohanKumar. "Effects of prenatal bisphenol-A exposure and postnatal overfeeding on cardiovascular function in female sheep." Journal of Developmental Origins of Health and Disease 8, no. 1 (November 4, 2016): 65–74. http://dx.doi.org/10.1017/s204017441600057x.

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Bisphenol-A (BPA) is a widely used endocrine-disrupting chemical. Prenatal exposure to BPA is known to affect birth weight, but its impact on the cardiovascular system has not been studied in detail. In this study, we investigated the effects of prenatal BPA treatment and its interaction with postnatal overfeeding on the cardiovascular system. Pregnant sheep were given daily subcutaneous injections of corn oil (control) or BPA (0.5 mg/kg/day in corn oil) from day 30 to day 90 of gestation. A subset of female offspring of these dams were overfed to increase body weight to ~30% over that of normal fed controls. Cardiovascular function was assessed using non-invasive echocardiography and cuff blood pressure (BP) monitoring at 21 months of age. Ventricular tissue was analyzed for gene expression of cardiac markers of hypertrophy and collagen at the end of the observation period. Prenatal BPA exposure had no significant effect on BP or morphometric measures. However, it increased atrial natriuretic peptide gene expression in the ventricles and reduced collagen expression in the right ventricle. Overfeeding produced a marked increase in body weight and BP. There were compensatory increases in left ventricular area and internal diameter. Prenatal BPA treatment produced a significant increase in interventricular septal thickness when animals were overfed. However, it appeared to block the increase in BP and left ventricular area caused by overfeeding. Taken together, these results suggest that prenatal BPA produces intrinsic changes in the heart that are capable of modulating morphological and functional parameters when animals become obese in later life.

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15

Juvet, C., U. Simeoni, C. Yzydorczyk, B. Siddeek, J. B. Armengaud, K. Nardou, P. Juvet, M. Benahmed, F. Cachat, and H. Chehade. "Effect of early postnatal nutrition on chronic kidney disease and arterial hypertension in adulthood: a narrative review." Journal of Developmental Origins of Health and Disease 9, no. 6 (August 6, 2018): 598–614. http://dx.doi.org/10.1017/s2040174418000454.

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AbstractIntrauterine growth restriction (IUGR) has been identified as a risk factor for adult chronic kidney disease (CKD), including hypertension (HTN). Accelerated postnatal catch-up growth superimposed to IUGR has been shown to further increase the risk of CKD and HTN. Although the impact of excessive postnatal growth without previous IUGR is less clear, excessive postnatal overfeeding in experimental animals shows a strong impact on the risk of CKD and HTN in adulthood. On the other hand, food restriction in the postnatal period seems to have a protective effect on CKD programming. All these effects are mediated at least partially by the activation of the renin–angiotensin system, leptin and neuropeptide Y (NPY) signaling and profibrotic pathways. Early nutrition, especially in the postnatal period has a significant impact on the risk of CKD and HTN at adulthood and should receive specific attention in the prevention of CKD and HTN.

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16

Sánchez-Garrido, M. A., J. M. Castellano, F. Ruiz-Pino, D. Garcia-Galiano, M. Manfredi-Lozano, S. Leon, A. Romero-Ruiz, C. Diéguez, L. Pinilla, and M. Tena-Sempere. "Metabolic Programming of Puberty: Sexually Dimorphic Responses to Early Nutritional Challenges." Endocrinology 154, no. 9 (June 10, 2013): 3387–400. http://dx.doi.org/10.1210/en.2012-2157.

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Body energy stores and metabolic cues influence the onset of puberty. However, the pubertal impact of early nutritional challenges has been only fragmentarily addressed. We evaluated here the consequences, in terms of pubertal timing and hormonal markers, of various nutritional manipulations during pre- or postnatal maturation in rats of both sexes. Males and females were submitted to gestational undernutrition (UNG) or peripubertal (SUB) subnutrition or were raised in large (LL; underfeeding) or small (SL; overfeeding) litters. In addition, groups of UNG, LL, and SL rats were fed on a high-fat diet (HFD) after weaning. Postnatal overfeeding resulted in higher body weights (BWs) during pubertal transition in both sexes, but only SL males displayed overtly advanced external signs of puberty. Postnatal underfeeding persistently decreased BW gain during puberty, yet the magnitude of pubertal delay was greater in LL males. In contrast, regardless of postnatal nutrition, HFD tended to advance the onset of puberty in females but did not alter pubertal timing in males. Likewise, SUB females displayed a marked delay in BW gain and puberty onset, whereas despite similar reduction in BW, SUB males showed normal timing of puberty. These sex divergences were also detected in various hormonal and metabolic indices so that postnatal overnutrition consistently increased LH, FSH, leptin, and insulin levels only in pubertal females, whereas HFD decreased gonadotropin levels in SL females but increased them in SL males. Notably, UNG rats did not show signs of delayed puberty but displayed a striking sex dimorphism in serum insulin/glucose levels, regardless of the diet, so that only UNG males had signs of presumable insulin resistance. Our data disclose important sex differences in the impact of various early nutritional challenges on the timing of puberty, which may help to explain the different trends of altered puberty and related comorbidities between sexes.

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17

SCHMIDT, INGRID, CORINNA SCHOELCH, THOMAS ZISKA, DARIUS SCHNEIDER, ECKHART SIMON, and ANDREAS PLAGEMANN. "Interaction of genetic and environmental programming of the leptin system and of obesity disposition." Physiological Genomics 3, no. 2 (August 9, 2000): 113–20. http://dx.doi.org/10.1152/physiolgenomics.2000.3.2.113.

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Schmidt, Ingrid, Corinna Schoelch, Thomas Ziska, Darius Schneider, Eckhart Simon, and Andreas Plagemann. Interaction of genetic and environmental programming for disturbances of the leptin system and for obesity. Physiol Genomics 3: 113–120, 2000.—Possible adverse interactions between an usually inconspicuous genetic trait and early environmental factors favoring the development of obesity were investigated in rats heterozygous for the leptin receptor defect “ fatty” ( fa). Pups were exposed to early postnatal overfeeding by reducing litter size from normally 10–12 to only 4. Rearing +/+ and +/ fa pups from day 3 to 21 in small litters increased fat-free dry mass and body fat, but only in the latter did a significant interaction with genotype occur. Pronounced differences in the responsiveness of +/+ and +/ fa pups to “prophylactic” leptin treatment (from day 1 to 21) were observed, with +/ fa females from small litters being nearly as fat and unresponsive as previously reported for normally reared fa/ fa pups. Clear heterozygous differences in total hypothalamic leptin binding, but no litter size effect, paralleling the differences in leptin responsiveness, were observed. By early postnatal overfeeding an usually inconspicuous genetic trait may thus become etiologic for the development of obesity via physiological changes other than the decreased leptin binding characterizing the genetic defect.

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18

Amaro, Andreia, Diana Sousa, Mariana Sá-Rocha, Marcos Divino Ferreira-Junior, Daniela Rosendo-Silva, Lucas Paulo Jacinto Saavedra, Cátia Barra, et al. "Postnatal Overfeeding in Rodents Induces a Neurodevelopment Delay and Anxious-like Behaviour Accompanied by Sex- and Brain-Region-Specific Synaptic and Metabolic Changes." Nutrients 15, no. 16 (August 15, 2023): 3581. http://dx.doi.org/10.3390/nu15163581.

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Nutritional disturbances during the early postnatal period can have long-lasting effects on neurodevelopment and may be related to behavioural changes at adulthood. While such neuronal connection disruption can contribute to social and behaviour alterations, the dysregulation of the neuroendocrine pathways involved in nutrient-sensing balance may also cause such impairments, although the underlying mechanisms are still unclear. We aimed to evaluate sex-specific neurodevelopmental and behavioural changes upon postnatal overfeeding and determine the potential underpinning mechanisms at the central nervous system level, with a focus on the interconnection between synaptic and neuroendocrine molecular alterations. At postnatal day 3 (PND3) litters were culled to three animals (small litter procedure). Neurodevelopmental tests were conducted at infancy, whereas behavioural tests to assess locomotion, anxiety, and memory were performed at adolescence, together with molecular analysis of the hippocampus, hypothalamus, and prefrontal cortex. At infancy, females presented impaired acquisition of an auditory response, eye opening, olfactory discrimination, and vestibular system development, suggesting that female offspring neurodevelopment/maturation was deeply affected. Male offspring presented a transitory delay in locomotor performance., while both offspring had lower upper limb strength. At adolescence, both sexes presented anxious-like behaviour without alterations in short-term memory retention. Both males and females presented lower NPY1R levels in a region-specific manner. Furthermore, both sexes presented synaptic changes in the hippocampus (lower GABAA in females and higher GABAA levels in males), while, in the prefrontal cortex, similar higher GABAA receptor levels were observed. At the hypothalamus, females presented synaptic changes, namely higher vGLUT1 and PSD95 levels. Thus, we demonstrate that postnatal overfeeding modulates offspring behaviour and dysregulates nutrient-sensing mechanisms such as NPY and GABA in a sex- and brain-region-specific manner.

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Lenon Klein, John, Sander Martinho Adams, Amanda Farias De Moura, Daniele Borchate, Dari Celestino Alves Filho, Dieison Pansiera Antunes, Fabiana Moro Maidana, Gilmar Dos SantosCardoso, Ivan Luiz Brondani, and Ricardo Gonçalves Gindri. "Efecto de la nutrición en el último tercio de la gestación de vacas de carne sobre el desarrollo de la progenie." Revista Mexicana de Ciencias Pecuarias 13, no. 3 (July 4, 2022): 658–73. http://dx.doi.org/10.22319/rmcp.v13i3.6015.

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The restriction of nutrient intake by beef cows during pregnancy may influence the progeny postpartum growth potential, therefore, the objective of the present study was to evaluate the effects of nutritional restriction and adequate nutrition or overfeeding during the final third of gestation of the crossbred cows (Charolais x Nellore) kept in the Pampa biome, on the productive performance of the progeny up to 15 mo of age. Eighty-three (83) cows were divided into: control cows on natural pasture under nutritional restriction (RES); Supplementation to meet 100 % of requirements (REQ); Supplementation above requirements (HIGH). REQ and HIGH calves had higher body weight at birth compared to calves from RES cows (39.28, 39.13 vs 34.58 kg), without influences on postnatal performance. Females from REQ and HIGH cows presented better postnatal performance and consequently higher weight at 12 mo of age in compared to offspring RES cows (300.71 and 311.79 vs 259.47 kg). These female calves reached 60 % of early adult weight (358 and 345 vs 405 d) and had a higher percentage of breeding at twelve months of age (73.98 and 84.08 vs 34.08 %) than females from RES cows. Supplementing cows to meet 100% requirements, as well as overfeeding during the final third of gestation, improves offspring performance at twelve months of age, with males and females responding differently to maternal nutritional insults during this period.

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20

Boubred, Farid, Christophe Buffat, Jean-Marc Feuerstein, Laurent Daniel, Michel Tsimaratos, Charles Oliver, Martine Lelièvre-Pégorier, and Umberto Simeoni. "Effects of early postnatal hypernutrition on nephron number and long-term renal function and structure in rats." American Journal of Physiology-Renal Physiology 293, no. 6 (December 2007): F1944—F1949. http://dx.doi.org/10.1152/ajprenal.00141.2007.

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Various antenatal events impair nephrogenesis in humans as well as in several animal models. The consecutive low nephron endowment may contribute to an increased risk for cardiovascular and renal diseases in adulthood. However, little knowledge is available on the influence of the postnatal environment, especially nutrition, on nephrogenesis. Moreover, the consequences of early postnatal nutrition in late adulthood are not clear. We used a model of early postnatal overfeeding (OF) induced by reduction of litter size (3 pups/litter) in rats. Systolic blood pressure (SBP; plethysmography), glomerular filtration rate (clearance of creatinine), glomerular number and volume, and glomerulosclerosis were evaluated in 22-mo-old aging offspring. Early postnatal OF was associated with increased weight gain during the suckling period (+40%, P < 0.01) and a 20% increase in glomerular number ( P < 0.05). However, an increase in SBP at 12 mo by an average of 18 mmHg and an increase in proteinuria (2.6-fold) and glomerulosclerosis at 22 mo of age were observed in OF male offspring compared with controls. In conclusion, early postnatal OF in the rat enhances postnatal nephrogenesis, but elevated blood pressure and glomerulosclerosis are still observed in male adults. Factors other than glomerular number reduction are likely to contribute to the arterial hypertension induced by early postnatal OF.

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Costa, V. M. G., A. E. Andreazzi, M. Bolotari, C. G. Lade, M. O. Guerra, and V. M. Peters. "Effect of postnatal overfeeding on the male and female Wistar rat reproductive parameters." Journal of Developmental Origins of Health and Disease 10, no. 6 (June 3, 2019): 667–75. http://dx.doi.org/10.1017/s2040174419000163.

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AbstractOverweight/obesity has become a worldwide epidemic, and factors such as a sedentary lifestyle and inadequate eating habits directly contribute to the development of this condition. Studies indicate that rapid weight gain at critical development stages, such as the lactation period, is associated with the development of obesity, cardiovascular diseases, and diabetes in the long term. In addition to metabolic changes during adulthood, overweight/obesity may influence reproductive function of the population. In this context, the present study aimed to evaluate postnatal overfeeding effects on male and female Wistar rat reproductive parameters. Postnatal overfeeding was induced by applying the litter reduction method for both sexes. Forty animals were used, divided into four groups: two with normal litters (NL♂ and NL♀) and two with small litters (SL♂ and SL♀). The males were euthanized at 90 days of age, on the same date the females were mated. Females were also euthanized after the 20-day gestation. Metabolic and reproductive variables were analyzed. Regarding males, SL animals showed increased body weight, adiposity, and decreased relative weight of the seminal vesicle, prostate, and epididymis as well as changes in the ITT and OGTT glycemic tests. Concerning females, SL animals presented increased body weight, relative perigonadal fat weight, glucose intolerance as well as modify the vaginal opening and increased weight of female pup. The litter reduction method was efficient in leading to metabolic and reproductive alterations in male and female Wistar rat.

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22

Dai, Yanyan, Nan Zhou, Fan Yang, Shanshan Zhou, Lijun Sha, Jianping Wang, and Xiaonan Li. "Effects of postnatal overfeeding and fish oil diet on energy expenditure in rats." Pediatric Research 83, no. 1 (October 4, 2017): 156–63. http://dx.doi.org/10.1038/pr.2017.207.

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Clarke, M. A., A. Stefanidis, and S. J. Spencer. "Postnatal Overfeeding Leads to Obesity and Exacerbated Febrile Responses to Lipopolysaccharide Throughout Life." Journal of Neuroendocrinology 24, no. 3 (February 23, 2012): 511–24. http://dx.doi.org/10.1111/j.1365-2826.2011.02269.x.

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Rodrigues, Ananda L., Érica P. G. De Souza, Simone V. Da Silva, Dayane S. B. Rodrigues, Aline B. Nascimento, Christina Barja-Fidalgo, and Marta S. De Freitas. "Low expression of insulin signaling molecules impairs glucose uptake in adipocytes after early overnutrition." Journal of Endocrinology 195, no. 3 (October 2, 2007): 485–94. http://dx.doi.org/10.1677/joe-07-0046.

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Experimental and clinical studies have demonstrated that early postnatal overnutrition represents a risk factor for later obesity and associated metabolic and cardiovascular disturbance. In the present study, we assessed the levels of glucose transporter 4 (GLUT-4), GLUT-1, insulin receptor (IR), IR substrate 1 (IRS-1), phosphatidylinositol 3-kinase (PI3K) and Akt expression, as well as insulin-stimulated glucose transport and Akt activity in adipocytes from adult rats previously raised in small litters (SL). The normal litter (NL) served as control group. We also investigated glycemia, insulinemia, plasma lipid levels, and glucose tolerance. Our data demonstrated that early postnatal overfeeding induced a persistent hyperphagia accompanied by a significant increase in body weight until 90 days of age. The SL group also presented a significant increase (∼42%) in epidydimal fat weight. Blood glucose, plasma insulin, and lipid levels were similar among the animals from the SL and NL groups. While insulin-stimulated glucose uptake was approximately twofold higher in adipocytes from the NL group, no stimulatory effect was observed in the SL group. The impaired insulin-stimulated glucose transport in adipose cells from the SL rats was associated with a significant decrease in GLUT-4, IRS-1 and PI3K expression, and Akt activity. In contrast, IR and Akt expression in adipocytes was not different between the SL and NL groups. Despite these alterations, our results showed no differences in glucose tolerance test in rats raised under different feeding conditions. Our findings reinforce a potent and long-term effect of neonatal overfeeding, which can program major changes in the metabolic regulatory mechanisms.

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Yzydorczyk, Catherine, Na Li, Eve Rigal, Hassib Chehade, Dolores Mosig, Jean Baptiste Armengaud, Thibaud Rolle, et al. "Calorie Restriction in Adulthood Reduces Hepatic Disorders Induced by Transient Postnatal Overfeeding in Mice." Nutrients 11, no. 11 (November 16, 2019): 2796. http://dx.doi.org/10.3390/nu11112796.

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Impaired early nutrition influences the risk of developing metabolic disorders in later life. We observed that transient postnatal overfeeding (OF) in mice induces long-term hepatic alterations, characterized by microsteatosis, fibrosis associated with oxidative stress (OS), and stress-induced premature senescence (SIPS). In this study, we investigated whether such changes can be reversed by moderate calorie restriction (CR). C57BL/6 male mice pups were maintained during lactation in litters adjusted to nine pups in the normal feeding (NF) group and three pups in the transient postnatal OF group. At six months of age, adult mice from the NF and OF groups were randomly assigned to an ad libitum diet or CR (daily energy supply reduced by 20%) for one month. In each group, at the age of seven months, analysis of liver structure, liver markers of OS (superoxide anion, antioxidant defenses), and SIPS (lipofuscin, p53, p21, p16, pRb/Rb, Acp53, sirtuin-1) were performed. CR in the OF group reduced microsteatosis, decreased levels of superoxide anion, and increased protein expression of catalase and superoxide dismutase. Moreover, CR decreased lipofuscin staining, p21, p53, Acp53, and p16 but increased pRb/Rb and sirtuin-1 protein expression. CR did not affect the NF group. These results suggest that CR reduces hepatic disorders induced by OF.

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Boubred, F., M. Saint-Faust, C. Buffat, I. Ligi, I. Grandvuillemin, and U. Simeoni. "Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis." International Journal of Nephrology 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/346067.

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Cardiovascular diseases are one of the leading causes of mortality. Hypertension (HT) is one of the principal risk factors associated with death. Chronic kidney disease (CKD), which is probably underestimated, increases the risk and the severity of adverse cardiovascular events. It is now recognized that low birth weight is a risk factor for these diseases, and this relationship is amplified by a rapid catch-up growth or overfeeding during infancy or childhood. The pathophysiological and molecular mechanisms involved in the “early programming” of CKD are multiple and partially understood. It has been proposed that the developmental programming of arterial hypertension and chronic kidney disease is related to a reduced nephron endowment. However, this mechanism is still discussed. This review discusses the complex relationship between birth weight and nephron endowment and how early growth and nutrition influence long term HT and CKD. We hypothesize that fetal environment reduces moderately the nephron number which appears insufficient by itself to induce long term diseases. Reduced nephron number constitutes a “factor of vulnerability” when additional factors, in particular a rapid postnatal growth or overfeeding, promote the early onset of diseases through a complex combination of various pathophysiological pathways.

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Peel, R. K., G. J. Eckerle, and R. V. Anthony. "Effects of overfeeding naturally-mated adolescent ewes on maternal, fetal, and postnatal lamb growth1." Journal of Animal Science 90, no. 11 (November 1, 2012): 3698–708. http://dx.doi.org/10.2527/jas.2012-5140.

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Davidowa, Helga, and Andreas Plagemann. "Inhibition by insulin of hypothalamic VMN neurons in rats overweight due to postnatal overfeeding." Neuroreport 12, no. 15 (October 2001): 3201–4. http://dx.doi.org/10.1097/00001756-200110290-00012.

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Boullu-Ciocca, S., V. Tassistro, A. Dutour, and M. Grino. "Pioglitazone in adult rats reverses immediate postnatal overfeeding-induced metabolic, hormonal, and inflammatory alterations." Endocrine 50, no. 3 (June 18, 2015): 608–19. http://dx.doi.org/10.1007/s12020-015-0657-z.

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Junior, Marcos Divino Ferreira, Keilah Valéria Naves Cavalcante, Lucas Araújo Ferreira, Paulo Ricardo Lopes, Carolina Nobre Ribeiro Pontes, Amanda de Sá Martins de Bessa, Ângela Ribeiro Neves, et al. "Postnatal early overfeeding induces cardiovascular dysfunction by oxidative stress in adult male Wistar rats." Life Sciences 226 (June 2019): 173–84. http://dx.doi.org/10.1016/j.lfs.2019.04.018.

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Tejera-Muñoz, Antonio, Lucía Guerra-Menéndez, Sara Amor, Daniel González-Hedström, Ángel Luis García-Villalón, and Miriam Granado. "Postnatal Overfeeding during Lactation Induces Endothelial Dysfunction and Cardiac Insulin Resistance in Adult Rats." International Journal of Molecular Sciences 24, no. 19 (September 22, 2023): 14443. http://dx.doi.org/10.3390/ijms241914443.

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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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Govoni, Kristen E., Sarah A. Reed, and Steven A. Zinn. "CELL BIOLOGY SYMPOSIUM: METABOLIC RESPONSES TO STRESS: FROM ANIMAL TO CELL: Poor maternal nutrition during gestation: effects on offspring whole-body and tissue-specific metabolism in livestock species1,2." Journal of Animal Science 97, no. 7 (May 9, 2019): 3142–52. http://dx.doi.org/10.1093/jas/skz157.

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Abstract Poor maternal nutrition, both restricted-feeding and overfeeding, during gestation can negatively affect offspring growth, body composition, and metabolism. The effects are observed as early as the prenatal period and often persist through postnatal growth and adulthood. There is evidence of multigenerational effects demonstrating the long-term negative impacts on livestock production. We and others have demonstrated that poor maternal nutrition impairs muscle growth, increases adipose tissue, and negatively affects liver function. In addition to altered growth, changes in key metabolic factors, increased glucose concentrations, insulin insensitivity, and hyperleptinemia are observed during the postnatal period. Furthermore, there is recent evidence of altered metabolism in specific tissues (e.g., muscle, adipose, and liver) and stem cells. The systemic and local changes in metabolism demonstrate the importance of determining the mechanism(s) by which maternal diet programs offspring growth and metabolism in an effort to develop novel management practices to improve the efficiency of growth and health in these offspring.

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Fabianová, Kamila, Janka Babeľová, Dušan Fabian, Alexandra Popovičová, Marcela Martončíková, Adam Raček, and Enikő Račeková. "Maternal High-Energy Diet during Pregnancy and Lactation Impairs Neurogenesis and Alters the Behavior of Adult Offspring in a Phenotype-Dependent Manner." International Journal of Molecular Sciences 23, no. 10 (May 16, 2022): 5564. http://dx.doi.org/10.3390/ijms23105564.

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Obesity is one of the biggest and most costly health challenges the modern world encounters. Substantial evidence suggests that the risk of metabolic syndrome or obesity formation may be affected at a very early stage of development, in particular through fetal and/or neonatal overfeeding. Outcomes from epidemiological studies indicate that maternal nutrition during pregnancy and lactation has a profound impact on adult neurogenesis in the offspring. In the present study, an intergenerational dietary model employing overfeeding of experimental mice during prenatal and early postnatal development was applied to acquire mice with various body conditions. We investigated the impact of the maternal high-energy diet during pregnancy and lactation on adult neurogenesis in the olfactory neurogenic region involving the subventricular zone (SVZ) and the rostral migratory stream (RMS) and some behavioral tasks including memory, anxiety and nociception. Our findings show that a maternal high-energy diet administered during pregnancy and lactation modifies proliferation and differentiation, and induced degeneration of cells in the SVZ/RMS of offspring, but only in mice where extreme phenotype, such as significant overweight/adiposity or obesity is manifested. Thereafter, a maternal high-energy diet enhances anxiety-related behavior in offspring regardless of its body condition and impairs learning and memory in offspring with an extreme phenotype.

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Achard, Vincent, Caroline Sanchez, Virginie Tassistro, Monique Verdier, Marie-Christine Alessi, and Michel Grino. "Immediate Postnatal Overfeeding in Rats Programs Aortic Wall Structure Alterations and Metalloproteinases Dysregulation in Adulthood." American Journal of Hypertension 29, no. 6 (November 6, 2015): 719–26. http://dx.doi.org/10.1093/ajh/hpv183.

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Plagemann, A., I. Heidrich, F. Götz, W. Rohde, and G. Dörner. "Obesity and Enhanced Diabetes and Cardiovascular Risk in Adult Rats due to Early Postnatal Overfeeding." Experimental and Clinical Endocrinology & Diabetes 99, no. 03 (July 16, 2009): 154–58. http://dx.doi.org/10.1055/s-0029-1211159.

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Rodrigues, Ananda Lages, Egberto Gaspar de Moura, Magna Cottini Fonseca Passos, Isis Hara Trevenzoli, Ellen Paula Santos da Conceição, Isabela Teixeira Bonono, José Firmino Nogueira Neto, and Patricia Cristina Lisboa. "Postnatal early overfeeding induces hypothalamic higher SOCS3 expression and lower STAT3 activity in adult rats." Journal of Nutritional Biochemistry 22, no. 2 (February 2011): 109–17. http://dx.doi.org/10.1016/j.jnutbio.2009.11.013.

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Habbout, Ahmed, Na Li, Luc Rochette, and Catherine Vergely. "Postnatal Overfeeding in Rodents by Litter Size Reduction Induces Major Short- and Long-Term Pathophysiological Consequences." Journal of Nutrition 143, no. 5 (February 27, 2013): 553–62. http://dx.doi.org/10.3945/jn.112.172825.

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Li, Na, Eve Rigal, Charles Guenancia, Luc Rochette, and Catherine Vergely. "0229: Alterations of cardiac function induced by postnatal overfeeding can be reversed by moderate diet restriction." Archives of Cardiovascular Diseases Supplements 6 (April 2014): 44. http://dx.doi.org/10.1016/s1878-6480(14)71382-5.

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Conceição, Ellen Paula Santos, Egberto Gaspar Moura, Elaine Oliveira, Deysla Sabino Guarda, Mariana Sarto Figueiredo, Fernanda Torres Quitete, Camila Calvino, et al. "Dietary calcium supplementation in adult rats reverts brown adipose tissue dysfunction programmed by postnatal early overfeeding." Journal of Nutritional Biochemistry 39 (January 2017): 117–25. http://dx.doi.org/10.1016/j.jnutbio.2016.09.013.

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Santos-Marcos, Jose A., Alexia Barroso, Oriol A. Rangel-Zuñiga, Cecilia Perdices-Lopez, Carmen Haro, Miguel A. Sanchez-Garrido, Helena Molina-Abril, et al. "Interplay between gonadal hormones and postnatal overfeeding in defining sex-dependent differences in gut microbiota architecture." Aging 12, no. 20 (October 27, 2020): 19979–20000. http://dx.doi.org/10.18632/aging.104140.

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Habbout, Ahmed, Stephanie Delemasure, Françoise Goirand, Jean-Claude Guilland, Franck Chabod, Mourad Sediki, Luc Rochette, and Catherine Vergely. "Postnatal overfeeding in rats leads to moderate overweight and to cardiometabolic and oxidative alterations in adulthood." Biochimie 94, no. 1 (January 2012): 117–24. http://dx.doi.org/10.1016/j.biochi.2011.09.023.

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42

Dai, Yanyan, Fan Yang, Nan Zhou, Lijun Sha, Shanshan Zhou, Junle Wang, and Xiaonan Li. "A post-weaning fish oil dietary intervention reverses adverse metabolic outcomes and 11β-hydroxysteroid dehydrogenase type 1 expression in postnatal overfed rats." British Journal of Nutrition 116, no. 9 (November 7, 2016): 1519–29. http://dx.doi.org/10.1017/s0007114516003718.

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AbstractEarly life is considered a critical period for determining long-term metabolic health. Postnatal over-nutrition may alter glucocorticoid (GC) metabolism and increase the risk of developing obesity and metabolic disorders in adulthood. Our aim was to assess the effects of the dose and timing of a fish oil diet on obesity and the expression of GC-activated enzyme 11β-hydroxysteroid dehydrogenase type 1 (HSD1) in postnatal overfed rats. Litter sizes were adjusted to three (small litter (SL)) or ten (normal litter) rats on postnatal day 3 to induce overfeeding or normal feeding. The SL rats were divided into three groups after weaning: high-dose fish oil (HFO), low-dose fish oil (LFO) and standard-diet groups. After 10 weeks, the HFO diet reduced body weight gain (16 %,P<0·05), improved glucose intolerance and decreased hyperlipaemia levels (P<0·05) in SL rats, but the LFO diet did not have any effect on the same rats. Moreover, we chose postnatal week 3 (W3), 6 (W6) and 8 (W8) as the intervention time points at which to begin the 10-week HFO diet, and found that the HFO diet improved glucose utilisation and lipid metabolism at all time points. However, body weight of SL rats was reversed to normal levels by the post-weaning intervention (461 (sem9·1)v. 450 (sem2·0)). 11β-HSD1 mRNA expression in the adipose tissue (49 (sem7·5)v. 161 (sem18·3),P<0·05) and hepatic tissue (11 (sem0·9)v. 16 (sem1·5),P<0·05) was decreased by the HFO diet at W3, but not at W6 or W8 (P>0·05). In conclusion, the post-weaning HFO diet could reverse adverse outcomes and decrease tissue GC activity in postnatal overfed rats.

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Veiga-Lopez, Almudena, Jacob Moeller, Rohit Sreedharan, Kanakadurga Singer, Carey Lumeng, Wen Ye, Anthony Pease, and Vasantha Padmanabhan. "Developmental programming: interaction between prenatal BPA exposure and postnatal adiposity on metabolic variables in female sheep." American Journal of Physiology-Endocrinology and Metabolism 310, no. 3 (February 1, 2016): E238—E247. http://dx.doi.org/10.1152/ajpendo.00425.2015.

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Among potential contributors for the increased incidence of metabolic diseases is the developmental exposure to endocrine-disrupting chemicals such as bisphenol A (BPA). BPA is an estrogenic chemical used in a variety of consumer products. Evidence points to interactions of BPA with the prevailing environment. The aim of this study was to assess the effects of prenatal exposure to BPA on postnatal metabolic outcomes, including insulin resistance, adipose tissue distribution, adipocyte morphometry, and expression of inflammatory markers in adipose tissue as well as to assess whether postnatal overfeeding would exacerbate these effects. Findings indicate that prenatal BPA exposure leads to insulin resistance in adulthood in the first breeder cohort ( study 1), but not in the second cohort ( study 2), which is suggestive of potential differences in genetic susceptibility. BPA exposure induced adipocyte hypertrophy in the visceral fat depot without an accompanying increase in visceral fat mass or increased CD68, a marker of macrophage infiltration, in the subcutaneous fat depot. Cohens effect size analysis found the ratio of visceral to subcutanous fat depot in the prenatal BPA-treated overfed group to be higher compared with the control-overfed group. Altogether, these results suggest that exposure to BPA during fetal life at levels found in humans can program metabolic outcomes that lead to insulin resistance, a forerunner of type 2 diabetes, with postnatal obesity failing to manifest any interaction with prenatal BPA relative to insulin resistance and adipocyte hypertrophy.

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Morris, M. J. "060. OVER FEEDING EARLY IN LIFE AND RISK OF OBESITY: INSIGHT FROM THE RODENT." Reproduction, Fertility and Development 21, no. 9 (2009): 15. http://dx.doi.org/10.1071/srb09abs060.

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While adult lifestyle factors undoubtedly contribute to the incidence of obesity and its attendant disorders, mounting evidence suggests that programming of obesity may occur following over-nutrition during development. As hypothalamic control of appetite and energy expenditure is set early in life and can be perturbed by certain exposures such as under-nutrition and altered metabolic and hormonal signals, in utero exposure to maternal obesity related changes may contribute to programming of obesity in offspring. Data from animal studies indicate both intrauterine and postnatal environments are critical determinants of the development of pathways regulating energy homeostasis. Experimental evidence in rat studies from our laboratory points to an additive detrimental impact of high fat diet consumption after weaning in animals born of obese mothers. Deleterious effects of high fat diet during pregnancy on metabolic profile, adiposity and cardiac hypertrophy were enhanced by postnatal over consumption. Even modest early postnatal overfeeding induced by litter size reduction leads to increased adiposity. Studies are needed to determine to what extent the effect of maternal and early nutritional changes persist. This presentation summarizes recent evidence of the impact of maternal obesity on subsequent obesity risk, paying particular attention to the hypothalamic regulation of appetite, and markers of metabolic control. There is an urgent need to investigate the mechanisms underlying the trans-generational effects of maternal obesity due to an extraordinary rise in the rates of maternal obesity.

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Ferreira, Lucas Araújo, Marcos Divino Ferreira-Junior, Keytiane de Jesus Viana Amaral, Keilah Valéria Naves Cavalcante, Carolina Nobre Ribeiro Pontes, Larissa Cristina dos Santos Ribeiro, Beatriz Gonçalves dos Santos, et al. "Maternal postnatal early overfeeding induces sex-related cardiac dysfunction and alters sexually hormones levels in young offspring." Journal of Nutritional Biochemistry 103 (May 2022): 108969. http://dx.doi.org/10.1016/j.jnutbio.2022.108969.

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Koneva, L. A., A. K. Vyas, R. C. McEachin, M. Puttabyatappa, H. S. Wang, M. A. Sartor, and V. Padmanabhan. "Developmental programming: Interaction between prenatal BPA and postnatal overfeeding on cardiac tissue gene expression in female sheep." Environmental and Molecular Mutagenesis 58, no. 1 (January 2017): 4–18. http://dx.doi.org/10.1002/em.22071.

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Rinaldi, Wilson, Rodrigo Gomes, Dionízia Scomparin, Sabrina Grassiolli, Tatiane Ribeiro, Gabriel Fabricio, Luiz Barella, et al. "Low-intensity and moderate exercise training improves autonomic nervous system activity imbalanced by postnatal early overfeeding in rats." Journal of the International Society of Sports Nutrition 11, no. 1 (2014): 25. http://dx.doi.org/10.1186/1550-2783-11-25.

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Li, Yuzhen, Andreas Plagemann, and Helga Davidowa. "Increased inhibition by agouti-related peptide of ventromedial hypothalamic neurons in rats overweight due to early postnatal overfeeding." Neuroscience Letters 330, no. 1 (September 2002): 33–36. http://dx.doi.org/10.1016/s0304-3940(02)00722-x.

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Rigal, Eve, Marie Josse, Geoffrey Dogon, Ivan Porcherot, Luc Rochette, Charles Guenancia, and Catherine Vergely. "Long-term impact of postnatal overfeeding on sensitivity to ischemia-reperfusion injury in vivo and on cardio-metabolism risk." Archives of Cardiovascular Diseases Supplements 14, no. 2 (June 2022): 167. http://dx.doi.org/10.1016/j.acvdsp.2022.04.029.

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Siddeek, B., N. Li, C. Yzydorczyk, C. Greco, U. Simeoni, and C. Vergely. "MIR-193B-Inflammasome: a potential pathway in adult cardiometabolic dysfunctions induced by postnatal overfeeding and target for their reversal." Archives of Cardiovascular Diseases Supplements 9, no. 2 (April 2017): 177. http://dx.doi.org/10.1016/s1878-6480(17)30439-1.

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