scholarly journals The Effect of Neonatal Leptin Treatment on Postnatal Weight Gain in Male Rats Is Dependent on Maternal Nutritional Status during Pregnancy

Endocrinology ◽  
2008 ◽  
Vol 149 (4) ◽  
pp. 1906-1913 ◽  
Author(s):  
Mark H. Vickers ◽  
Peter D. Gluckman ◽  
Alice H. Coveny ◽  
Paul L. Hofman ◽  
Wayne S. Cutfield ◽  
...  
Keyword(s):  
Weight Gain ◽  
Nutritional Status ◽  
Energy Homeostasis ◽  
Caloric Intake ◽  
Developmental Trajectory ◽  
Male Offspring ◽  
Male Rats ◽  
Metabolic Phenotype ◽  
Chow Diet

An adverse prenatal environment may induce long-term metabolic consequences, in particular obesity, hyperleptinemia, insulin resistance, and type 2 diabetes. Although the mechanisms are unclear, this “programming” has generally been considered an irreversible change in developmental trajectory. Adult offspring of rats subjected to undernutrition (UN) during pregnancy develop obesity, hyperinsulinemia, and hyperleptinemia, especially in the presence of a high-fat diet. Using this model of maternal UN, we have recently shown that neonatal leptin treatment in females reverses the postnatal sequelae induced by developmental programming. To examine possible gender-related effects of neonatal leptin treatment, the present study investigated the effect of neonatal leptin treatment on the metabolic phenotype of adult male offspring. Leptin treatment (recombinant rat leptin, 2.5 μg/g·d, sc) from postnatal d 3–13 resulted in a transient slowing of neonatal weight gain, particularly in programmed offspring. Neonatal leptin treatment of male offspring from normally nourished mothers caused an increase in diet-induced weight gain and related metabolic sequelae, including hyperinsulinemia and increased total body adiposity compared with saline-treated controls. This occurred without an increase in caloric intake. These effects were specific to offspring of normal pregnancies and were not observed in offspring of mothers after UN during pregnancy. In the latter, neonatal leptin treatment conferred protection against the development of the programmed phenotype, particularly in those fed the chow diet postnatally. These data further reinforce the importance of leptin in determining long-term energy homeostasis, and suggest that leptin’s effects are modulated by gender and both prenatal and postnatal nutritional status.

scholarly journals Catecholaminergic projections into an interconnected forebrain network control the sensitivity of male rats to diet-induced obesity

2018 ◽  
Vol 314 (6) ◽  
pp. R811-R823 ◽  
Author(s):  
Shin J. Lee ◽  
Anne J. Jokiaho ◽  
Graciela Sanchez-Watts ◽  
Alan G. Watts
Keyword(s):  
Visceral Fat ◽  
Energy Homeostasis ◽  
Network Control ◽  
Visceral Adiposity ◽  
Male Rats ◽  
Chow Diet ◽  
Corticosterone Secretion ◽  
Increase Food Intake ◽  
Glucagon Like Peptide 1

Hindbrain catecholamine neurons convey gut-derived metabolic signals to an interconnected neuronal network in the hypothalamus and adjacent forebrain. These neurons are critical for short-term glycemic control, glucocorticoid and glucoprivic feeding responses, and glucagon-like peptide 1 (GLP-1) signaling. Here we investigate whether these pathways also contribute to long-term energy homeostasis by controlling obesogenic sensitivity to a high-fat/high-sucrose choice (HFSC) diet. We ablated hindbrain-originating catecholaminergic projections by injecting anti-dopamine-β-hydroxylase-conjugated saporin (DSAP) into the paraventricular nucleus of the hypothalamus (PVH) of male rats fed a chow diet for up to 12 wk or a HFSC diet for 8 wk. We measured the effects of DSAP lesions on food choices; visceral adiposity; plasma glucose, insulin, and leptin; and indicators of long-term ACTH and corticosterone secretion. We also determined lesion effects on the number of carbohydrate or fat calories required to increase visceral fat. Finally, we examined corticotropin-releasing hormone levels in the PVH and arcuate nucleus expression of neuropeptide Y ( Npy), agouti-related peptide ( Agrp), and proopiomelanocortin ( Pomc). DSAP-injected chow-fed rats slowly increase visceral adiposity but quickly develop mild insulin resistance and elevated blood glucose. DSAP-injected HFSC-fed rats, however, dramatically increase food intake, body weight, and visceral adiposity beyond the level in control HFSC-fed rats. These changes are concomitant with 1) a reduction in the number of carbohydrate calories required to generate visceral fat, 2) abnormal Npy, Agrp, and Pomc expression, and 3) aberrant control of insulin secretion and glucocorticoid negative feedback. Long-term metabolic adaptations to high-carbohydrate diets, therefore, require intact forebrain catecholamine projections. Without them, animals cannot alter forebrain mechanisms to restrain increased visceral adiposity.

scholarly journals Neonatal nutritional programming impairs adiponectin effects on energy homeostasis in adult life of male rats

2018 ◽  
Vol 315 (1) ◽  
pp. E29-E37 ◽  
Author(s):  
Mariana Peduti Halah ◽  
Paula Beatriz Marangon ◽  
Jose Antunes-Rodrigues ◽  
Lucila L. K. Elias
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
White Adipose Tissue ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Adult Life ◽  
Male Rats ◽  
Nutritional Programming

Neonatal nutritional changes induce long-lasting effects on energy homeostasis. Adiponectin influences food intake and body weight. The aim of this study was to investigate the effects of neonatal nutritional programming on the central stimulation of adiponectin. Male Wistar rats were divided on postnatal (PN) day 3 in litters of 3 (small litter, SL), 10 (normal litter, NL), or 16 pups/dam (large litter, LL). We assessed body weight gain for 60 days, adiponectin concentration, and white adipose tissue weight. We examined the response of SL, NL, and LL rats on body weight gain, food intake, oxygen consumption (V̇o2), respiratory exchange ratio (RER), calorimetry, locomotor activity, phosphorylated-AMP-activated protein kinase (AMPK) expression in the hypothalamus, and uncoupling protein (UCP)-1 in the brown adipose tissue after central stimulus with adiponectin. After weaning, SL rats maintained higher body weight gain despite similar food intake compared with NL rats. LL rats showed lower body weight at weaning, with a catch up afterward and higher food intake. Both LL and SL groups had decreased plasma concentrations of adiponectin at PN60. SL rats had increased white adipose tissue. Central injection of adiponectin decreased body weight and food intake and increased V̇o2, RER, calorimetry, p-AMPK and UCP- 1 expression in NL rats, but it had no effect on SL and LL rats, compared with the respective vehicle groups. In conclusion, neonatal under- and overfeeding induced an increase in body weight gain in juvenile and early adult life. Unresponsiveness to central effects of adiponectin contributes to the imbalance of the energy homeostasis in adult life induced by neonatal nutritional programming.

Prevention of diet-induced obesity and impaired glucose tolerance in rats following administration of leptin to their mothers

2007 ◽  
Vol 292 (5) ◽  
pp. R1810-R1818 ◽  
Author(s):  
Claire J. Stocker ◽  
Ed Wargent ◽  
Jacqueline O'Dowd ◽  
Claire Cornick ◽  
John R. Speakman ◽  
...  
Keyword(s):  
Weight Gain ◽  
Energy Balance ◽  
Glucose Tolerance ◽  
Female Offspring ◽  
Male Offspring ◽  
Male Rats ◽  
Fat Pad ◽  
Plasma Insulin Concentration ◽  
Obesogenic Diet ◽  
Tolerance Curve

Absence of leptin is known to disrupt the development of energy balance regulatory mechanisms. We investigated whether administration of leptin to normally nourished rats affects energy balance in their offspring. Leptin (2 mg·kg−1·day−1) was administered from day 14 of pregnancy and throughout lactation. Male and female offspring were fed either on chow or on high-fat diets that elicited similar levels of obesity in the sexes from 6 wk to 15 mo of age. Treatment of the dams with leptin prevented diet-induced increases in the rate of weight gain, retroperitoneal fat pad weight, area under the intraperitoneal glucose tolerance curve, and fasting plasma insulin concentration in female offspring. In the male offspring, the diet-induced increase in weight gain was prevented and increased fat pad weight was reduced. Energy intake per rat was higher in response to the obesogenic diet in male offspring of saline-treated but not leptin-treated dams. A similar trend was seen in 3-mo-old female offspring. Energy expenditure at 3 mo of age was higher for a given body weight in female offspring of leptin-treated compared with saline-treated dams when these animals were fed on the obesogenic diet. A similar trend was seen for male rats fed on the obesogenic diet. Thus leptin levels during pregnancy and lactation can affect the development of energy balance regulatory systems in their offspring.

scholarly journals Combined Deletion of Y1, Y2, and Y4 Receptors Prevents Hypothalamic Neuropeptide Y Overexpression-Induced Hyperinsulinemia despite Persistence of Hyperphagia and Obesity

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5094-5101 ◽  
Author(s):  
En-Ju D. Lin ◽  
Amanda Sainsbury ◽  
Nicola J. Lee ◽  
Dana Boey ◽  
Michelle Couzens ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Neuropeptide Y ◽  
Energy Homeostasis ◽  
Viral Vector ◽  
Body Weight Gain ◽  
Hormonal Changes ◽  
Obesity Syndrome ◽  
Y Receptors

Neuropeptide Y (NPY) is a key regulator of energy homeostasis and is implicated in the development of obesity and type 2 diabetes. Whereas it is known that hypothalamic administration of exogenous NPY peptides leads to increased body weight gain, hyperphagia, and many hormonal and metabolic changes characteristic of an obesity syndrome, the Y receptor(s) mediating these effects is disputed and unclear. To investigate the role of different Y receptors in the NPY-induced obesity syndrome, we used recombinant adeno-associated viral vector to overexpress NPY in mice deficient of selective single or multiple Y receptors (including Y1, Y2, and Y4). Results from this study demonstrated that long-term hypothalamic overexpression of NPY lead to marked hyperphagia, hypogonadism, body weight gain, enhanced adipose tissue accumulation, hyperinsulinemia, and other hormonal changes characteristic of an obesity syndrome. NPY-induced hyperphagia, hypogonadism, and obesity syndrome persisted in all genotypes studied (Y1−/−, Y2−/−, Y2Y4−/−, and Y1Y2Y4−/− mice). However, triple deletion of Y1, Y2, and Y4 receptors prevented NPY-induced hyperinsulinemia. These findings suggest that Y1, Y2, and Y4 receptors under this condition are not crucially involved in NPY’s hyperphagic, hypogonadal, and obesogenic effects, but they are responsible for the central regulation of circulating insulin levels by NPY.

Corrigendum to: IGF-I is not a useful marker for nutritional status in the growing pig under commercial conditions

2001 ◽  
Vol 52 (7) ◽  
pp. 791
Author(s):  
L. Ma ◽  
F. R. Dunshea ◽  
Y. M. Brockwell ◽  
R. L. Inglis ◽  
D. J. Kingston ◽  
...  
Keyword(s):  
Weight Gain ◽  
Nutritional Status ◽  
Dietary Protein ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Low Protein ◽  
Igf I ◽  
Protein Diets

Plasma hormone concentrations were measured in gilts after fasting, long-term protein restriction, or supplementation. In 11-week-old pigs fasted overnight, plasma insulin, glucagon, gastrin, urea, and glucose were increased 30 min after re-feeding (P < 0.05), whereas IGF-I did not change. In 16-week-old gilts fed a standard commercial diet [14.6% crude protein (CP)], or a high-protein diet (16.7% CP) for 4 weeks, the high-protein diet increased weight gain (13%; P < 0.05) and carcass weight (4%; P < 0.05), but did not alter plasma IGF-I, insulin, or glucagon. In 10-week-old gilts fed high-protein diets (19.4% and 18.3% CP), or low-protein diets (15.5% and 13.3% CP) for 12 weeks during the grower and finisher phases, respectively, the low-protein diet decreased weight gain (18%; P < 0.001) and carcass weight (11%; P < 0.01), with a marked increase in plasma glucagon (P < 0.05), no change in insulin, and only a trend towards decreased IGF-I (P = 0.1). The pigs were more sensitive to altered dietary protein at 10 weeks of age than at 16 weeks. Plasma IGF-I was not responsive to the short-term effects of feeding or the long-term effects of dietary protein. Glucagon could provide a useful marker for nutritional status in young pigs, provided that time of feeding is taken into account.

Early postnatal overfeeding induces early chronic renal dysfunction in adult male rats

2009 ◽  
Vol 297 (4) ◽  
pp. F943-F951 ◽  
Author(s):  
Farid Boubred ◽  
Laurent Daniel ◽  
Christophe Buffat ◽  
Jean-Marc Feuerstein ◽  
Michel Tsimaratos ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Renal Dysfunction ◽  
Postnatal Growth ◽  
Male Offspring ◽  
Male Rats ◽  
Nephron Number

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.

scholarly journals Effect of nicotine on body composition in mice

2011 ◽  
Vol 212 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Michael Mangubat ◽  
Kabirullah Lutfy ◽  
Martin L Lee ◽  
Laura Pulido ◽  
David Stout ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Partial Agonist ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Fat Distribution ◽  
Abdominal Fat ◽  
Chow Diet ◽  
Fat Composition

Nicotine induces weight loss in both humans and rodents consuming a regular diet; however, the effect of nicotine on body weight and fat composition in rodents consuming a high-fat diet (HFD) has not been well studied. Thus, this study examined the effect of nicotine vs saline on body weight and fat composition in mice fed with either an HFD (62% of kcal from fat) or a standard normal chow diet (NCD) for 7 weeks. Nicotine dose dependently reduced body weight gain in mice that consumed both diets, but this effect was significantly greater in mice on the HFD. Caloric intake was decreased in nicotine-treated mice. Estimates of energy intake suggested that decreased caloric intake accounted for all the reduced weight gain in mice on an NCD and 66% of the reduced weight gain on an HFD. Computed tomography analysis for fat distribution demonstrated that nicotine was effective in reducing abdominal fat in mice that consumed the HFD, with nicotine treatment leading to lower visceral fat. The effect of nicotine on weight loss in mice on an HFD was completely blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor (nAChR) antagonist, but only partially blocked by the α4β2 nAChR partial agonist/antagonist, varenicline. We conclude that nicotine is effective in preventing HFD-induced weight gain and abdominal fat accumulation.

scholarly journals Petite Integration Factor 1 (PIF1) helicase deficiency increases weight gain in Western diet-fed female mice without increased inflammatory markers or decreased glucose clearance

2018 ◽  
Author(s):  
Frances R. Belmonte ◽  
Nikolaos Dedousis ◽  
Ian Sipula ◽  
Nikita A. Desai ◽  
Aatur D. Singhi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Gain ◽  
Hepatic Steatosis ◽  
Inflammatory Markers ◽  
Western Diet ◽  
Metabolic Phenotype ◽  
Whole Body ◽  
Chow Diet ◽  
Female Mice ◽  
Glucose Clearance

AbstractPetite Integration Factor 1 (PIF1) is a multifunctional helicase present in nuclei and mitochondria. PIF1 knock out (KO) mice exhibit accelerated weight gain and decreased wheel running on a normal chow diet. In the current study, we investigated whether Pif1 removal alters whole body metabolism in response to weight gain. PIF1 KO and wild type (WT) C57BL/6J mice were fed a Western diet (WD) rich in fat and carbohydrates before evaluation of their metabolic phenotype. Compared with weight gain-resistant WT female mice, WD-fed PIF1 KO females, but not males, showed accelerated adipose deposition, decreased locomotor activity, and reduced whole-body energy expenditure without increased dietary intake. Surprisingly, PIF1 KO females were protected against obesity-induced alterations in fasting blood glucose and glucose clearance. WD-fed PIF1 KO females developed mild hepatic steatosis and associated changes in liver gene expression that were absent in weight-matched, WD-fed female controls, linking hepatic steatosis to Pif1 ablation rather than increased body weight. WD-fed PIF1 KO females also showed decreased gene expression of inflammatory markers in adipose tissue. Collectively, these data separated weight gain from inflammation and impaired glucose homeostasis. They also support a role for Pif1 in weight gain resistance and liver metabolic dysregulation during nutrient stress.

scholarly journals La ingesta de stevia modifica la dinámica del peso corporal, la glucosa y el colesterol en ratas hembras: Algoritmo k-NNs

2020 ◽  
Vol 70 (2) ◽  
pp. 144-151
Author(s):  
María del Rocío Padilla Galindo ◽  
Alma Gabriela Martínez Moreno ◽  
Fatima Ezzahra Housni ◽  
Zyanya Reyes Castillo ◽  
Erika Saenz-Pardo Reyes
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
The Body ◽  
Female Rats ◽  
Male Rats ◽  
Predictive Analysis ◽  
Free Access ◽  
Glucose Levels

El consumo de stevia ha sido promovido por su bajo aporte calórico, su efecto antidiabético y antihipercolesterolémico. Sin embargo, los efectos de la ingesta de stevia parecen no ser los mismos para las ratas hembras respecto de los machos. El propósito de este estudio fue evaluar el efecto de la ingesta de stevia sobre el consumo de alimento, peso corporal y niveles de glucosa, insulina, colesterol y triglicéridos en ratas hembras Wistar durante 13 semanas y realizar un análisis predictivo del peso corporal y la ingesta de alimento a 20 semanas. Se utilizaron 20 ratas hembras adultas, que se dividieron en 2 grupos: control (CG) y stevia (SG), ambos grupos recibieron agua y comida a libre acceso, así como una solución de stevia al 0,2 % para el grupo SG. Se registró diariamente el consumo de alimento, agua y solución de stevia; la medición del peso corporal se realizó semanalmente. Al final de las 13 semanas de experimentación, los animales se sacrificaron para evaluar los parámetros metabolicos. El grupo SG mostró un mayor consumo de alimento, mayor proporción de ganancia de peso corporal, niveles de glucosa y colesterol que el grupo CG. No se encontraron diferencias significativas en los niveles de triglicéridos e insulina. Respecto al análisis predictivo (semanas 14-20), se mantiene un incremento significativo en el consumo de alimento y se observa una tendencia de aumento en la proporción de ganancia de peso corporal. Esto indica que el consumo de stevia en ratas hembras parece no tener los mismos efectos benéficos reportados en machos. Consumption of stevia has been promoted due to its low caloric intake, it’s effects as anti-diabetic and anti-hypercholesterolemic. However, the effects of stevia consumption is apparently not the same in females than males. The purpose of this study was to evaluate the effect of stevia intake on meal consumption, body weight and levels of glucose, insulin, cholesterol and triglycerides in female Wistar rats during 13 weeks and develop a predictive analysis of the body weight and meal intake over 20 weeks. 20 adult female rats were utilized, these were divided into two groups: control (CG) and stevia (SG), both groups received free access to water and food, the SG also received a stevia solution at 0.2%. Consumption of food, water and stevia solution was recorded daily, while weight was recorded weekly. At the end of the 13 weeks of experiment, the subjects were sacrificed to evaluate the metabolic parameters. The SG group showed a higher consumption of food, higher proportion of body weight gain, glucose levels and cholesterol than the CG. No significant differences were found in levels of triglyceride or insulin. Respect to the predictive analysis (weeks 14-20), a significant increase in food consumption is maintained and an increasing trend is observed in the proportion of body weight gain. This indicates that stevia consumption appears not to have the same benefit effects in female rats than male rats.

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