Seasonal obesity in Syrian hamsters: effects of age, diet, photoperiod, and melatonin

1984 ◽  
Vol 247 (2) ◽  
pp. R328-R334 ◽  
Author(s):  
G. N. Wade ◽  
T. J. Bartness

Two experiments examined the effects of photoperiod, melatonin, and diet on body weight in female Syrian hamsters (Mesocricetus auratus). In experiment 1, daily injections of 25 micrograms melatonin increased body weight when given 3 h before lights-out but not when given at the midpoint of the light phase, in a 16-h light-8-h dark cycle (LD 16:8). Ten micrograms of melatonin, given 3 h before lights-out, were sufficient to increase body weight and fat content, to increase interscapular brown adipose tissue weight, to decrease uterine weight, and to interrupt estrous cyclicity. However, 2.5 micrograms of melatonin increased body weight and fat content without affecting brown adipose tissue weight or reproductive function. In experiment 2, melatonin treatment, exposure to a short photoperiod (LD 8:16), and feeding a high-fat diet increased body weight gain in weanling (25-day-old) female hamsters. When melatonin treatment or high-fat diet were withdrawn, hamsters reduced their food intake, and their body weight and fat content returned to control levels. After 15-17 wk in the short photoperiod, hamsters also began to undereat, and their body weight and fat content returned to control levels. These findings suggest several conclusions. 1) As with the changes in reproductive function, melatonin is effective at increasing body weight only when given at certain times of day. 2) Not all end points are equally responsive to melatonin, suggesting that they are independent of one another. 3) Weanling hamsters respond to photoperiod, melatonin, and diet just as adults do. 4) The striking obesities induced by these manipulations are completely reversible.

2012 ◽  
Vol 518-523 ◽  
pp. 498-501
Author(s):  
Ke Yue Liu

Effects of the ethanol extracts prepared from Salix babylonica L. leaves on the fat deposit induced in mice by feeding a high-fat-diet for 9 wks were studied. Increase in body weight and parametrial adipose tissue weight containing 2,5 or 10g (extract) /kg food was suppressed as compared to that observed in mice fed the high-fat-diet alone. Futhermore, the enthanol extract inhibited the elevation of blood triacylglycerol in rats administered orally a lipid emulsion as compared to that in rats given the emulsion alone. Experiments are now undergoing to isolate other ingredients from the extract and test them for anti-obesity effects.


Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2501
Author(s):  
Maihemuti Mijiti ◽  
Ryosuke Mori ◽  
Bingyu Huang ◽  
Kenichiro Tsukamoto ◽  
Keisuke Kiriyama ◽  
...  

Dietary protamine can ameliorate hyperlipidemia; however, the protamine-derived active peptide and its hypolipidemic mechanism of action are unclear. Here, we report the discovery of a novel anti-obesity and hypocholesterolemic peptide, RPR (Arg-Pro-Arg), derived from protamine in mice fed a high-fat diet for 50 days. Serum cholesterol levels were significantly lower in the protamine and RPR groups than in the control group. White adipose tissue weight was significantly decreased in the protamine and RPR groups. The fecal excretion of cholesterol and bile acid was significantly higher in the protamine and RPR groups than in the control group. We also observed a significant decrease in the expression of hepatic SCD1, SREBP1, and adipocyte FAS mRNA, and significantly increased expression of hepatic PPARα and adipocyte PPARγ1 mRNA in the protamine group. These findings demonstrate that the anti-obesity effects of protamine are linked to the upregulation of adipocyte PPARγ1 and hepatic PPARα and the downregulation of hepatic SCD1 via SREBP1 and adipocyte FAS. RPR derived from protamine has a crucial role in the anti-obesity action of protamine by evaluating the effective dose of adipose tissue weight loss.


2005 ◽  
Vol 288 (6) ◽  
pp. E1236-E1243 ◽  
Author(s):  
Elena Velkoska ◽  
Timothy J. Cole ◽  
Margaret J. Morris

Early life nutrition impacts on subsequent risk of obesity and hypertension. Several brain chemicals responsible for both feeding and cardiovascular regulation are altered in obesity. We examined effects of early postnatal overnutrition on blood pressure, brain neuropeptide Y (NPY), and adiposity markers. Rat pup litters were adjusted to either 3 or 12 male animals (overnutrition and control, respectively) on day 1 of life. After weaning, rats were given either a palatable high-fat diet or standard chow. Smaller litter pups were significantly heavier by 17 days of age. By 16 wk, the effect of litter size was masked by that of diet, postweaning. Small and normal litter animals fed a high-fat diet had similar increases in body weight, plasma insulin, leptin, and adiponectin concentrations, leptin mRNA, and fat masses relative to chow-fed animals. An increase in 11β-hydroxysteroid dehydrogenase-1 mRNA in white adipose tissue, and a decrease in uncoupling protein-1 mRNA in brown adipose tissue in both small litter groups at 16 wk of age, may represent a programming effect of the altered litter size. NPY concentration in the paraventricular nucleus of the hypothalamus was reduced in high fat-fed groups. Blood pressure was significantly elevated at 13 wk in high-fat-fed animals. This study demonstrates that overnourishment during early postnatal development leads to profound changes in body weight at weaning, which tended to abate with maturation. Thus the effects of long-term dietary intervention postweaning can override those of litter size-induced obesity.


1984 ◽  
Vol 246 (6) ◽  
pp. R943-R948 ◽  
Author(s):  
J. Oku ◽  
G. A. Bray ◽  
J. S. Fisler ◽  
R. Schemmel

The effects of ventromedial hypothalamic (VMH) knife-cut lesions on food intake and body weight of S 5B/Pl rats, which are normally resistant to obesity when eating a high-fat diet, were examined in two experiments. In the first experiment body weight increased only slightly after VMH knife-cut lesions when animals were fed pelleted laboratory chow or a 10% corn oil diet. When eating the 30% corn oil diet, however, body weight increased in the VMH knife-cut rats. In the second experiment VMH knife-cut lesions produced a small weight gain in rats fed the 10% fat diet; this manipulation also increased food intake and disrupted the normal diurnal feeding pattern. Changes in the weight of the liver, interscapular brown adipose tissue, and white adipose tissue paralleled the changes in body weight. Plasma insulin increased in the rats eating the 30% corn oil diet ad libitum but not in the VMH-lesioned animals pair fed to the sham-operated rats. Incorporation of 3H from 3H2O into lipid was significantly increased in white fat of animals with VMH knife cuts. Similar results were obtained from incubation of adipose tissue in vitro with insulin and radioactively labeled glucose. These studies show that hypothalamic knife-cut lesions can remove the resistance of the S 5B/Pl rats to obesity when they are fed a high-fat diet.


2013 ◽  
Vol 77 (1) ◽  
pp. 53-57 ◽  
Author(s):  
Yukako OKAZAKI ◽  
Novita Vivi SITANGGANG ◽  
Satoko SATO ◽  
Nanae OHNISHI ◽  
Junji INOUE ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 560 ◽  
Author(s):  
Ran Okouchi ◽  
Yuto Sakanoi ◽  
Tsuyoshi Tsuduki

We investigated whether the difference in miso consumption between the Japanese diets of 1975 and 2010 has influenced the observed increase in diet-induced obesity. To recreate the 2010 and 1975 Japanese high-fat diets with the corresponding proportions of miso, freeze-dried miso was added to high-fat mouse feed at 1.6% and 2.6%, respectively. When 5-week-old male Institute of Cancer Research (ICR) mice were provided each of these diets ad libitum for 8 weeks, it was found that the white adipose tissue weight and adipocyte area were lower in mice receiving the 1975 diet than in those receiving the 2010 diet. Therefore, high miso consumption is one reason why the 1975 Japanese diet tended to not lead to obesity. Next, the combined effects of treadmill exercise and miso consumption were investigated. The mice were divided into three groups, which were provided either a high-fat diet (group C), a high-fat diet with exercise (group C + E), or a miso-supplemented high-fat diet with exercise (group M + E) for 8 weeks. In this experiment, the white adipose tissue weight and adipocyte area in group M + E were lower than in group C. When the mRNA expression of lipid metabolism-associated genes in adipose tissue was measured, we found that expression of Hsl (lipase, hormone sensitive), which is involved in lipolysis, and Pparγ (peroxisome proliferator activated receptor gamma), which regulates adipocyte differentiation upstream of Hsl, was increased in group M + E. These results clearly demonstrated that lipid accumulation in the adipose tissues is suppressed by miso consumption in combination with exercise.


1982 ◽  
Vol 30 (1) ◽  
pp. 15 ◽  
Author(s):  
CR Tidemann

Information on seasonal changes in activity, body weight and brown adipose tissue weight was collected from a wild population of a small Australian vespertilionid, Eptesicus vulturnus. Both sexes, but especially females, became less active during the colder months of the year. Males maintained body weight and brown adipose tissue weight during winter, as do non-hibernating mammals. Females lost brown adipose tissue and body weight during winter, as do hibernators. The relationship between the sex differences in overwintering behaviour and the reproductive cycle is discussed.


Endocrinology ◽  
2014 ◽  
Vol 156 (2) ◽  
pp. 411-418 ◽  
Author(s):  
Pierre Cardinal ◽  
Luigi Bellocchio ◽  
Omar Guzmán-Quevedo ◽  
Caroline André ◽  
Samantha Clark ◽  
...  

The paraventricular nucleus of the hypothalamus (PVN) regulates energy balance by modulating not only food intake, but also energy expenditure (EE) and brown adipose tissue thermogenesis. To test the hypothesis that cannabinoid type 1 (CB1) receptor in PVN neurons might control these processes, we used the Cre/loxP system to delete CB1 from single-minded 1 (Sim1) neurons, which account for the majority of PVN neurons. On standard chow, mice lacking CB1 receptor in Sim1 neurons (Sim1-CB1-knockout [KO]) had food intake, body weight, adiposity, glucose metabolism, and EE comparable with wild-type (WT) (Sim1-CB1-WT) littermates. However, maintenance on a high-fat diet revealed a gene-by-diet interaction whereby Sim1-CB1-KO mice had decreased adiposity, improved insulin sensitivity, and increased EE, whereas feeding behavior was similar to Sim1-CB1-WT mice. Additionally, high-fat diet-fed Sim1-CB1-KO mice had increased mRNA expression of the β3-adrenergic receptor, as well as of uncoupling protein-1, cytochrome-c oxidase subunit IV and mitochondrial transcription factor A in the brown adipose tissue, all molecular changes suggestive of increased thermogenesis. Pharmacological studies using β-blockers suggested that modulation of β-adrenergic transmission play an important role in determining EE changes observed in Sim1-CB1-KO. Finally, chemical sympathectomy abolished the obesity-resistant phenotype of Sim1-CB1-KO mice. Altogether, these findings reveal a diet-dependent dissociation in the CB1 receptor control of food intake and EE, likely mediated by the PVN, where CB1 receptors on Sim1-positive neurons do not impact food intake but hinder EE during dietary environmental challenges that promote body weight gain.


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