scholarly journals Diet-Induced Obesity in Mice Overexpressing Neuropeptide Y in Noradrenergic Neurons

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Suvi T. Ruohonen ◽  
Laura H. Vähätalo ◽  
Eriika Savontaus
Keyword(s):  
Weight Gain ◽  
Neuropeptide Y ◽  
Transgenic Mouse Model ◽  
Noradrenergic Neurons ◽  
Fat Depots ◽  
Diet Induced Obesity ◽  
Cholesterol Levels ◽  
Insulin Tolerance ◽  
Normal Chow ◽  
Obesity In Mice

Neuropeptide Y (NPY) is a neurotransmitter associated with feeding and obesity. We have constructed an NPY transgenic mouse model (OE- mouse), where targeted overexpression leads to increased levels of NPY in noradrenergic and adrenergic neurons. We previously showed that these mice become obese on a normal chow. Now we aimed to study the effect of a Western-type diet in OE- and wildtype (WT) mice, and to compare the genotype differences in the development of obesity, insulin resistance, and diabetes. Weight gain, glucose, and insulin tolerance tests, fasted plasma insulin, and cholesterol levels were assayed. We found that female OE- mice gained significantly more weight without hyperphagia or decreased activity, and showed larger white and brown fat depots with no difference in UCP-1 levels. They also displayed impaired glucose tolerance and decreased insulin sensitivity. OE- and WT males gained weight robustly, but no difference in the degree of adiposity was observed. However, 40% of but none of the WT males developed hyperglycaemia while on the diet. The present study shows that female OE- mice were not protected from the obesogenic effect of the diet suggesting that increased NPY release may predispose females to a greater risk of weight gain under high caloric conditions.

scholarly journals PARP1 deficiency exacerbates diet-induced obesity in mice

2010 ◽  
Vol 205 (3) ◽  
pp. 243-252 ◽  
Author(s):  
Kishor Devalaraja-Narashimha ◽  
Babu J Padanilam
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Food Intake ◽  
Heat Production ◽  
Diet Induced Obesity ◽  
Insulin Tolerance ◽  
Protein Functions ◽  
Normal Chow ◽  
Obesity In Mice ◽  
Fat Reabsorption

Poly (ADP-ribose) polymerase-1 (PARP1) regulates gene expression as a transcriptional cofactor and protein functions via poly (ADP-ribosyl)ation. This study was aimed to determine the effect of Parp1 gene deficiency on diet-induced obesity and energy metabolism. Parp1-knockout (Parp-KO) and wild-type (WT) mice on the same genetic background were fed either normal chow or high-fat (HF) diet. Food intake and weight gain were monitored weekly. Plasma levels of glucose, leptin, and insulin were monitored monthly. At 19 weeks, locomotor activity, body composition, respiratory quotient and heat production, glucose and insulin tolerance, and fat reabsorption were analyzed. Parp-KO mice are highly susceptible to diet-induced obesity, accumulation of fat tissue, and they develop hyperleptinemia and insulin resistance and glucose intolerance compared with their WT counterparts. The increased weight gain is due to decreased metabolic rate, heat production, and total energy expenditure (EE). Paradoxically, food intake is less, and the motor activity and oxidation of fat are higher in Parp-KO mice. Absorption of fatty acids is not altered between the groups after HF diet. These results suggest that malfunction of PARP1 signaling exacerbates diet-induced obesity, hyperleptinemia, and insulin resistance, and that it decreases EE in 129 mice.

scholarly journals Effects of Vitamin E Supplementation to Metabolic Markers on Diet-Induced Obesity in Mice 

Folia Medica ◽  
2021 ◽  
Vol 63 (6) ◽  
pp. 895-900
Author(s):  
Eka Roina Megawati ◽  
Lokot Donna Lubis ◽  
Febi Yanti Harahap
Keyword(s):  
Body Weight ◽  
Vitamin E ◽  
Blood Sugar ◽  
Adiponectin Level ◽  
Metabolic Markers ◽  
Diet Induced Obesity ◽  
Cholesterol Levels ◽  
Significant Difference ◽  
Obesity In Mice ◽  
Vitamin E Supplementation

Introduction: Obesity creates health problems by increasing the risks of chronic diseases such as type 2 diabetes and cardiovascular disorders. Obesity leads to insulin resistance, higher blood glucose and cholesterol levels. Adipose tissues synthesize adiponectin which acts as anti-inflammatory, antidiabetic, and anti-atherogenic agent. Meanwhile, vitamin E is an antioxidant that acts as an anti-inflammation. Aim: The purpose of this study was to analyze the effects of vitamin E supplementation to metabolic markers on diet-induced obesity in mice. Materials and methods: Twenty-four mice (Mus musculus, L) aged four weeks were divided into six groups which were fed different diets and given vitamin E in different dosages or methods. The period of treatment was 18 weeks. The mice body weights were measured every week; blood sugar and cholesterol levels were measured every six weeks, and the adiponectin level measurement was done at week 18. Results: A repeated measures ANOVA showed that body weight and cholesterol level within groups were not significantly different [F(15, 54)=1.417, 0.173 and F(10, 36)=1.391, 0.224 respectively]. The glucose levels were found to be significantly different [F(7.646, 27.526)=2.625, 0.030]. There was no significant difference in the adiponectin levels. Conclusions: Vitamin E supplementation could not prevent the increase of body weight, the elevation of blood sugar and cholesterol levels, and also could not increase adiponectin level.

scholarly journals Propolis Prevents Diet-Induced Hyperlipidemia and Mitigates Weight Gain in Diet-Induced Obesity in Mice

2009 ◽  
Vol 32 (12) ◽  
pp. 2022-2028 ◽  
Author(s):  
Satomi Koya-Miyata ◽  
Norie Arai ◽  
Akiko Mizote ◽  
Yoshifumi Taniguchi ◽  
Shimpei Ushio ◽  
...  
Keyword(s):  
Weight Gain ◽  
Diet Induced Obesity ◽  
Obesity In Mice

scholarly journals Prostaglandin PGE2 receptor EP4 regulates microglial phagocytosis and increases susceptibility to diet-induced obesity

2021 ◽  
Author(s):  
Anzela Niraula ◽  
Rachael D Fasnacht ◽  
Kelly M Ness ◽  
Jeremy M Frey ◽  
Mauricio D Dorfman ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Microglial Activation ◽  
Body Weight Gain ◽  
Microglial Phagocytosis ◽  
Diet Induced Obesity ◽  
Insulin Tolerance ◽  
Pge2 Receptor

Background: In rodents, susceptibility to diet-induced obesity requires microglial activation, but the molecular components of this pathway remain incompletely defined. Prostaglandin E2 (PGE2) levels increase in the mediobasal hypothalamus during high fat diet (HFD) feeding, and the PGE2 receptor EP4 regulates microglial activation state and phagocytic activity, suggesting a potential role for microglial EP4 signaling in obesity pathogenesis. Method: Metabolic phenotyping, as assessed by body weight, energy expenditure, glucose, and insulin tolerance, was performed in microglia-specific EP4 knockout (MG-EP4 KO) mice and littermate controls on HFD. Morphological and gene expression analysis of microglia, and a histological survey of microglia-neuron interactions in the arcuate nucleus was performed. Phagocytosis was assessed using in vivo and in vitro pharmacological techniques. Results: Microglial EP4 deletion markedly reduced weight gain and food intake in response to HFD feeding. In correspondence with this lean phenotype, insulin sensitivity was also improved in the HFD-fed MG-EP4 KO mice though glucose tolerance remained surprisingly unaffected. Mechanistically, EP4-deficient microglia showed an attenuated phagocytic state marked by reduced CD68 expression and fewer contacts with POMC neuron soma and processes. These cellular changes observed in the microglial EP4 knockout mice corresponded with an increased density of POMC neurites extending into the paraventricular nucleus. Conclusion: These findings reveal that microglial EP4 signaling promotes body weight gain and insulin resistance during HFD feeding. Furthermore, the data suggest that curbing microglial phagocytic function may preserve POMC cytoarchitecture and PVN input to limit overconsumption during diet-induced obesity.

Resistance to Diet-Induced Obesity in Mice Lacking OPA1 in Adipose Tissue Occurs Independently of Fat-Derived FGF-21 and BAT Function

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 276-LB ◽  
Author(s):  
RENATA PEREIRA ◽  
ANGELA C. OLVERA ◽  
ALEX A. MARTI ◽  
RANA HEWEZI ◽  
WILLIAM A. BUI TRAN ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Diet Induced Obesity ◽  
Obesity In Mice

White- and Brown-Rice Supplementation Improves Insulin Tolerance, Brown Fat Activation, Energy Expenditure, and Changes the Gut Microflora in Diet-Induced Obesity

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1897-P
Author(s):  
HISASHI YOKOMIZO ◽  
ATSUSHI ISHIKADO ◽  
TAKANORI SHINJO ◽  
KYOUNGMIN PARK ◽  
YASUTAKA MAEDA ◽  
...  
Keyword(s):  
Activation Energy ◽  
Energy Expenditure ◽  
Brown Rice ◽  
Brown Fat ◽  
Gut Microflora ◽  
Diet Induced Obesity ◽  
Insulin Tolerance

1759-P: Prostaglandin PGE2 Receptor EP4 Signaling Deficiency in Microglia Reduces Weight Gain with Transient Glucose Improvements in Diet-Induced Obesity

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1759-P
Author(s):  
ANZELA NIRAULA ◽  
RACHAEL FASNACHT ◽  
KELLY M. NESS ◽  
JEREMY FREY ◽  
MAURICIO D. DORFMAN ◽  
...  
Keyword(s):  
Weight Gain ◽  
Diet Induced Obesity ◽  
Pge2 Receptor
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