Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and Pomc gene expression reverts extreme obesity

The present study was aimed to investigate the mechanism underlying the influence of maternal low-protein (LP) diet on offspring growth in the chicken. One hundred and twenty Chinese inbred Langshan breeder hens were allocated randomly into two groups fed diets containing low (10 %, LP) or normal (15 %) crude protein levels. Low dietary protein did not affect the body weight of hens, but significantly decreased the laying rate and egg weight. The yolk leptin content was significantly lower in eggs laid by LP hens, while no differences were detected for yolk contents of corticosterone, tri-iodothyronine (T3) or thyroxine. Despite significantly lower hatch weight, the LP offspring demonstrated obviously higher serum T3 concentration, which is in accordance with the faster post-hatch growth rate achieving significantly heavier body weight and pectoralis major muscle weight 4 weeks post-hatching. Expression of 20-hydroxysteroid dehydrogenase (20-HSD) mRNA in the yolk-sac membrane was significantly down-regulated at embryonic day 14, whereas that of transthyretin and leptin receptor (LepR) was not altered. Moreover, hypothalamic expression of 20-HSD, glucocorticoid receptors, thyrotropin-releasing hormone and LepR mRNA was significantly up-regulated in the LP group compared with their control counterparts. In the pectoralis major muscle, significantly higher expression of insulin-like growth factor (IGF)-I and IGF-I receptor mRNA was observed in LP embryos. The present study provides evidence that maternal LP diet programmes post-hatch growth of the offspring. The associated alterations in yolk leptin deposition as well as in yolk-sac membrane, fetal hypothalamus and muscle gene expression may be involved in mediating such programming effect in the chicken.

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Early Weaning Affects Liver Antioxidant Function in Piglets

Animals ◽

10.3390/ani11092679 ◽

2021 ◽

Vol 11 (9) ◽

pp. 2679

Author(s):

Lihuai Yu ◽

Hongmin Li ◽

Zhong Peng ◽

Yuzhu Ge ◽

Jun Liu ◽

...

Keyword(s):

Gene Expression ◽

Body Weight ◽

Antioxidant Enzymes ◽

Liver Weight ◽

The Body ◽

Early Weaning ◽

Large White ◽

Enzymes Activity ◽

Antioxidant Function ◽

The Impact

This study examined the impact of early weaning on antioxidant function in piglets. A total of 40 Duroc × Landrace × Large White, 21-day-old piglets (half male and half female) were divided into suckling groups (SG) and weaning groups (WG). Piglets in WG were weaned at the 21st day, while the piglets in SG continued to get breastfed. Eight piglets from each group were randomly selected and slaughtered at 24th-day (SG3, WG3) and 28th-day old (SG7, WG7). The body weight, liver index, hepatocyte morphology, antioxidant enzymes activity, gene expression of antioxidant enzymes, and Nrf2 signaling in the liver of piglets were measured. The results showed that weaning caused decreased body weight (p < 0.01), lower liver weight (p < 0.01), and decreased the liver organ index (p < 0.05) of piglets. The area and size of hepatocytes in the WG group was smaller than that in the SG group (p < 0.05). We also observed that weaning reduced the activity of superoxide dismutase (SOD) and catalase (CAT) (p < 0.05) in the liver of piglets. Relative to the SG3 group, the gene expression of GSH-Px in liver of WG3 was significantly reduced (p < 0.05). The gene expression of Nrf2 in the SG3 group was higher than that in the WG3 group (p < 0.01). The gene expression of NQO1 in the SG7 group was higher than that in the WG7 group (p < 0.05). In conclusion, weaning resulted in lower weight, slowed liver development, and reduced antioxidant enzymes activity, thereby impairing liver antioxidant function and suppressing piglet growth.

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The Body Weight-related Differences of Leptin and Neuropeptide Y (NPY) Gene Expression in Pigs

Asian-Australasian Journal of Animal Sciences ◽

10.5713/ajas.2008.70260 ◽

2008 ◽

Vol 21 (2) ◽

pp. 161-166 ◽

Cited By ~ 2

Author(s):

Tizhong Shan ◽

Yizhen Wang ◽

Jia Guo ◽

Xiaona Chu ◽

Jianxin Liu ◽

...

Keyword(s):

Gene Expression ◽

Body Weight ◽

Neuropeptide Y ◽

The Body

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Metabolic Defense of the Body Weight Set Point

Psychiatric Annals ◽

10.3928/0048-5713-19831101-03 ◽

1983 ◽

Vol 13 (11) ◽

pp. 839-842 ◽

Cited By ~ 1

Author(s):

Richard E Keesey ◽

Stephen W Corbett

Keyword(s):

Body Weight ◽

The Body ◽

Set Point

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Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00117.2007 ◽

2007 ◽

Vol 293 (3) ◽

pp. R1056-R1062 ◽

Cited By ~ 123

Author(s):

Jacqueline Férézou-Viala ◽

Anne-France Roy ◽

Colette Sérougne ◽

Daniel Gripois ◽

Michel Parquet ◽

...

Keyword(s):

Body Weight ◽

Weight Gain ◽

Body Weight Gain ◽

Maternal Diet ◽

The Body ◽

Female Rats ◽

Leptin Resistance ◽

High Fat ◽

Leptin Sensitivity ◽

The Impact

Epidemiological and animal studies suggest that the alteration of hormonal and metabolic environment during fetal and neonatal development can contribute to development of metabolic syndrome in adulthood. In this paper, we investigated the impact of maternal high-fat (HF) diet on hypothalamic leptin sensitivity and body weight gain of offspring. Adult Wistar female rats received a HF or a control normal-fat (C) diet for 6 wk before gestation until the end of the suckling period. After weaning, pups received either C or HF diet during 6 wk. Body weight gain and metabolic and endocrine parameters were measured in the eight groups of rats formed according to a postweaning diet, maternal diet, and gender. To evaluate hypothalamic leptin sensitivity in each group, STAT-3 phosphorylation was measured in response to leptin or saline intraperitoneal bolus. Pups exhibited similar body weights at birth, but at weaning, those born to HF dams weighed significantly less (−12%) than those born to C dams. When given the HF diet, males and females born to HF dams exhibited smaller body weight and feed efficiency than those born to C dams, suggesting increased energy expenditure programmed by the maternal HF diet. Thus, maternal HF feeding could be protective against adverse effects of the HF diet as observed in male offspring of control dams: overweight (+17%) with hyperleptinemia and hyperinsulinemia. Furthermore, offspring of HF dams fed either C or HF diet exhibited an alteration in hypothalamic leptin-dependent STAT-3 phosphorylation. We conclude that maternal high-fat diet programs a hypothalamic leptin resistance in offspring, which, however, fails to increase the body weight gain until adulthood.

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Acute, but not chronic, exercise lowers the body weight set-point in male rats

Physiology & Behavior ◽

10.1016/0031-9384(92)90478-k ◽

1992 ◽

Vol 52 (6) ◽

pp. 1173-1177 ◽

Cited By ~ 7

Author(s):

M. Cabanac ◽

J. Morrissette

Keyword(s):

Body Weight ◽

The Body ◽

Male Rats ◽

Chronic Exercise ◽

Set Point

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Liraglutide, a GLP-1 Receptor Agonist, Which Decreases Hypothalamic 5-HT2A Receptor Expression, Reduces Appetite and Body Weight Independently of Serotonin Synthesis in Mice

Journal of Diabetes Research ◽

10.1155/2018/6482958 ◽

2018 ◽

Vol 2018 ◽

pp. 1-6 ◽

Cited By ~ 3

Author(s):

Katsunori Nonogaki ◽

Takao Kaji

Keyword(s):

Gene Expression ◽

Weight Loss ◽

Body Weight ◽

Receptor Agonist ◽

Tryptophan Hydroxylase ◽

Intraperitoneal Administration ◽

Body Weight Loss ◽

Receptor Activation ◽

The Body ◽

Receptor Expression

A recent report suggested that brain-derived serotonin (5-HT) is critical for maintaining weight loss induced by glucagon-like peptide-1 (GLP-1) receptor activation in rats and that 5-HT2A receptors mediate the feeding suppression and weight loss induced by GLP-1 receptor activation. Here, we show that changes in daily food intake and body weight induced by intraperitoneal administration of liraglutide, a GLP-1 receptor agonist, over 4 days did not differ between mice treated with the tryptophan hydroxylase (Tph) inhibitor p-chlorophenylalanine (PCPA) for 3 days and mice without PCPA treatment. Treatment with PCPA did not affect hypothalamic 5-HT2A receptor expression. Despite the anorexic effect of liraglutide disappearing after the first day of treatment, the body weight loss induced by liraglutide persisted for 4 days in mice treated with or without PCPA. Intraperitoneal administration of liraglutide significantly decreased the gene expression of hypothalamic 5-HT2A receptors 1 h after injection. Moreover, the acute anorexic effects of liraglutide were blunted in mice treated with the high-affinity 5-HT2A agonist (4-bromo-3,6-dimethoxybenzocyclobuten-1-yl) methylamine hydrobromide 14 h or 24 h before liraglutide injection. These findings suggest that liraglutide reduces appetite and body weight independently of 5-HT synthesis in mice, whereas GLP-1 receptor activation downregulates the gene expression of hypothalamic 5-HT2A receptors.

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