Long-term melatonin treatment attenuates body weight gain with aging in female mice.

2021 ◽  
Author(s):  
Isao Tamura ◽  
Hiroshi Tamura ◽  
Mai Kawamoto-Jozaki ◽  
Yumiko Doi-tanaka ◽  
Haruka Takagi ◽  
...  

Women usually experience body weight gain with aging, which can put them at risk for many chronic diseases. Previous studies indicated that melatonin treatment attenuates body weight gain and abdominal fat deposition in several male animals. However, it is unclear whether melatonin affects female animals in the same way. This study investigated whether long-term melatonin treatment can attenuate body weight gain with aging and, if it does, what the mechanism is. Ten-week-old female ICR mice were given melatonin-containing water (100 μg/mL) or water only until 43 weeks. Melatonin treatment significantly attenuated body weight gain at 23 weeks (control; 57.2±2.0 g vs. melatonin; 44.4±3.1 g), 33 weeks (control; 65.4±2.6 g vs. melatonin; 52.2±4.2 g) and 43 weeks (control; 66.1±3.2 g vs. melatonin; 54.4±2.5 g) without decreasing the amount of food intake. Micro-CT analyses showed that melatonin significantly decreased the deposition of visceral and subcutaneous fat. These results suggested that melatonin attenuates body weight gain by inhibiting abdominal fat deposition. Metabolome analysis of the liver revealed that melatonin treatment induced a drastic change in the metabolome with the down-regulation of 149 metabolites, including the metabolites of glucose and amino acids. Citrate, which serves as a source of de novo lipogenesis, was one of the down-regulated metabolites. These results show that long-term melatonin treatment induces drastic changes of metabolism and attenuates body weight gain and fat deposition with aging in female mice.

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5094-5101 ◽  
Author(s):  
En-Ju D. Lin ◽  
Amanda Sainsbury ◽  
Nicola J. Lee ◽  
Dana Boey ◽  
Michelle Couzens ◽  
...  

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.


Metabolism ◽  
2012 ◽  
Vol 61 (6) ◽  
pp. 812-822 ◽  
Author(s):  
Esther Fuente-Martín ◽  
Miriam Granado ◽  
Cristina García-Cáceres ◽  
Miguel A. Sanchez-Garrido ◽  
Laura M. Frago ◽  
...  

2017 ◽  
Vol 49 (06) ◽  
pp. 457-465 ◽  
Author(s):  
Ashley Russell ◽  
Jamie Grimes ◽  
Danette Cruthirds ◽  
Joanna Westerfield ◽  
Lawren Wooten ◽  
...  

Abstract17β-Estradiol is known to regulate energy metabolism and body weight. Ovariectomy results in body weight gain while estradiol administration results in a reversal of weight gain. Isoflavones, found in rodent chow, can mimic estrogenic effects making it crucial to understand the role of these compounds on metabolic regulation. The goal of this study is to examine the effect of dietary isoflavones on body weight regulation in the ovariectomized rat. This study will examine how dietary isoflavones can interact with estradiol treatment to affect body weight. Consistent with previous findings, animals fed an isoflavone-rich diet had decreased body weight (p<0.05), abdominal fat (p<0.05), and serum leptin levels (p<0.05) compared to animals fed an isoflavone-free diet. Estradiol replacement resulted in decreased body weight (p<0.05), abdominal fat (p<0.05), and serum leptin (p<0.05). Current literature suggests the involvement of cytokines in the inflammatory response of body weight gain. We screened a host of cytokines and chemokines that may be altered by dietary isoflavones or estradiol replacement. Serum cytokine analysis revealed significant (p<0.05) diet-dependent increases in inflammatory cytokines (keratinocyte-derived chemokine). The isoflavone-free diet in OVX rats resulted in the regulation of the following cytokines and chemokines: interleukin-10, interleukin-18, serum regulated on activation, normal T cell expressed and secreted, and monocyte chemoattractant protein-1 (p<0.05). Overall, these results reveal that estradiol treatment can have differential effects on energy metabolism and body weight regulation depending on the presence of isoflavones in rodent chow.


2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Ashley R. Chandler ◽  
Michelina M. Messina ◽  
J. Michael Overton

1990 ◽  
Vol 124 (3) ◽  
pp. 381-386 ◽  
Author(s):  
M. J. Gardner ◽  
D. J. Flint

ABSTRACT Treatment of neonatal rats on days 2–5 with antibodies against rat GH (rGH) markedly reduced body weight gain and serum concentrations of insulin-like growth factor-I for 6–8 weeks in both females and males, after which weight gain normalized without evidence of catch-up growth. There were no significant effects on serum prolactin, tri-iodothyronine or corticosterone. Testis and ovarian weights were reduced, although only in proportion to body size. In females, but not males, the treated rats, though lighter, had increased fat deposition in the parametrial depot. Pituitary weight was considerably reduced over 100 days later, as was the pituitary content of GH, but not prolactin. The response to GH-releasing factor of both male and female rats was also greatly reduced at this time. Taken together with the fact that these rGH antibodies can bind directly to somatotrophs, we propose that the long-term effects of the antibodies are induced by specific somatotroph destruction. Journal of Endocrinology (1990) 124, 381–386


2012 ◽  
Vol 92 (13) ◽  
pp. 2638-2643 ◽  
Author(s):  
Haiyan Chen ◽  
Yiling Wang ◽  
Lichuan Ma ◽  
Jiajun Zhao ◽  
Yinyin Li ◽  
...  

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