Melanin‐concentrating hormone neurons affect adipose tissues and modulate weight gain

2021 ◽  
Author(s):  
Clarissa M. D. Mota
Keyword(s):  
Weight Gain ◽  
Adipose Tissues ◽  
Melanin Concentrating Hormone

Poster #T48 INVESTIGATION OF THE PRO-MELANIN-CONCENTRATING HORMONE GENE IN ANTIPSYCHOTIC INDUCED WEIGHT GAIN

2014 ◽  
Vol 153 ◽  
pp. S306 ◽  
Author(s):  
Nabilah Chowdhury ◽  
Arun Tiwari ◽  
Eva Brandl ◽  
Jeffrey Lieberman ◽  
Herbert Y. Meltzer ◽  
...  
Keyword(s):  
Weight Gain ◽  
Melanin Concentrating Hormone

scholarly journals Flattened circadian glucocorticoid oscillations cause obesity due to increased lipid turnover and lipid uptake

2020 ◽  
Author(s):  
Stefan Tholen ◽  
Kyle M. Kovary ◽  
Atefeh Rabiee ◽  
Ewa Bielczyk-Maczyńska ◽  
Wenting Yang ◽  
...  
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Weight Gain ◽  
Lipid Accumulation ◽  
Body Weight Gain ◽  
List Type ◽  
Acid Uptake ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
White Fat

ABSTRACTChronic stressors flatten circadian glucocorticoid (GC) oscillations, which has been correlated with negative health outcomes including obesity. How such flattened circadian GC oscillations affect metabolism and fat storage remains unknown. Here we investigated the consequences in mice and found that flattening of GC oscillations results not only in body weight gain, mainly due to increases in white fat depot mass, but also leads to hyperinsulinemia and fat accumulation in brown adipose tissue. A transcriptomic analysis of white and brown adipose tissues revealed that flattened GC oscillations cause dysregulated lipid metabolism with a prominent role of the fatty acid transporter Cd36. Indeed, Cd36 knockout mice are partially protected against the adverse effects of flattened GC oscillations including body weight gain and lipid accumulation in the brown and visceral white fat depots. These results provide insights on how conditions associated with flattened GC levels cause obesity.HIGHLIGHTSFlattening of circadian GC oscillations in mice, despite keeping mean circulating GC levels the same, results in body weight gain, lipid accumulation in both brown and white adipose tissues (BAT and WAT), and hyperinsulinemia.Markedly, flattening GC oscillations for short periods of three days is sufficient to increase lipid accumulation and mass in BAT, but longer periods are needed to increase lipid accumulation and mass in WAT.Transcriptomics analysis shows increased expression of a key regulator of fatty acid uptake, CD36, and knockout of CD36 partially protects cells from flattening GC oscillations

Effect of rate of weight gain of steers during the stocker phase. III. Gene expression of adipose tissues and skeletal muscle in growing–finishing beef cattle1

2014 ◽  
Vol 92 (4) ◽  
pp. 1462-1472 ◽  
Author(s):  
P. A. Lancaster ◽  
E. D. Sharman ◽  
G. W. Horn ◽  
C. R Krehbiel ◽  
J. D. Starkey
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Weight Gain ◽  
Phase Iii ◽  
Adipose Tissues

scholarly journals Lithium and methylphenidate: opposite effects on perirenal brown fat

2010 ◽  
Vol 32 (2) ◽  
pp. 35-37
Author(s):  
José Menna Oliveira ◽  
Leonardo Machado Crema ◽  
Luísa Amália Diehl ◽  
Letícia Ferreira Pettenuzzo ◽  
Liane Tavares Bertinette ◽  
...  
Keyword(s):  
Weight Gain ◽  
Tissue Distribution ◽  
Adult Male ◽  
Wistar Rats ◽  
Brown Fat ◽  
Adult Rats ◽  
Adipose Tissues ◽  
Male Wistar Rats ◽  
Perirenal Fat

OBJECTIVE: To evaluate the effects of the administration of lithium to adult rats on brown (perirenal) and white (inguinal) adipose tissues and to assess whether methylphenidate modulates lithium effects. METHODS: Twenty-five adult male Wistar rats were fed with either regular or lithium-containing chow for 30 days. Between days 15 to 30 of treatment, animals received daily intraperitoneal administrations of either methylphenidate or saline. RESULTS: Lithium significantly reduced perirenal fat, and this effect was minimized by the administration of methylphenidate. There were no significant differences between the groups in terms of the effects of lithium on inguinal fat. CONCLUSION: Our findings suggest that different effects on white and brown tissue distribution may be involved in lithium-induced weight gain.

scholarly journals Overexpression of nuclear receptor SHP in adipose tissues affects diet-induced obesity and adaptive thermogenesis

2010 ◽  
Vol 298 (5) ◽  
pp. E961-E970 ◽  
Author(s):  
Imene Tabbi-Anneni ◽  
Robert Cooksey ◽  
Viswanath Gunda ◽  
Shiguo Liu ◽  
Aubrey Mueller ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Nuclear Receptor ◽  
Fat Mass ◽  
Cold Exposure ◽  
Metabolic Rates ◽  
Adipose Tissues ◽  
Fat Mass Index ◽  
Adaptive Thermogenesis ◽  
Diet Induced Obesity

The orphan nuclear receptor small heterodimer partner (SHP) regulates metabolic pathways involved in hepatic bile acid production and both lipid and glucose homeostasis via the transcriptional repression of other nuclear receptors. In the present study, we generated fat-specific SHP-overexpressed transgenic (TG) mice and determined the potential role of SHP activation, specifically in adipocytes, in the regulation of adipose tissue function in response to stressors. We determined in 2 mo-old SHP TG mice body weight, fat mass index, adipose tissues morphology, thermogenic and metabolic gene expression, metabolic rates at baseline and in response to β adrenergic receptor agonists, and brown fat ultrastructural changes in response to cold exposure (6–48 h). Mice were fed a 10-wk high-fat diet (HFD; 42% fat). Weight gain, fat mass index, adipose tissues morphology, glucose tolerance, and metabolic rates were determined at the end of the feeding. Young TG mice had increased body weight and adiposity; however, their energy metabolism was increased and brown fat function was enhanced in response to cold exposure through the activation of thermogenic genes and mitochondrial biogenesis. SHP overexpression exacerbated the diet-induced obesity phenotype as evidence by marked weight gain over time, increased adiposity, and severe glucose intolerance compared with wild-type mice fed a HFD. In addition, SHP-TG mice fed HFD had decreased diet-induced adaptive thermogenesis, increased food intake, and decreased physical activity. In conclusion, SHP activation in adipocytes strongly affects weight gain and diet-induced obesity. Developing a synthetic compound to antagonize the effect of SHP may prove to be useful in treating obesity.

scholarly journals Enhancement of Lipid Metabolism and Hepatic Stability in Fat-Induced Obese Mice by Fermented Cucurbita moschata Extract

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Md. Akil Hossain ◽  
Seung-Jin Lee ◽  
Na-Hye Park ◽  
Biruk Tesfaye Birhanu ◽  
Abraham Fikru Mechesso ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Fatty Liver ◽  
Liver Enzymes ◽  
Plasma Lipids ◽  
Body Weight Gain ◽  
Cucurbita Moschata ◽  
Obese Mice ◽  
Adipose Tissues ◽  
Lipogenic Genes

The aim of this study was to evaluate the potentials of fermented Cucurbita moschata extract (FCME) in the treatment of obesity and nonalcoholic fatty liver disease (NAFLD). Five-week-old male C57BL/6 mice were assigned to 6 groups and treated for 8 weeks by feeding the normal diet (ND) and high fat diet (HFD) with and without FCME. Changes in body weight gain and consumption of feed and water were recorded. Major organs, adipose tissues, and blood samples were collected after the experimental period. The serum lipid profile, histological features of liver and adipose tissues, and mRNA expression of different adipogenic/lipogenic genes from liver tissue were evaluated. The supplementation of FCME in HFD significantly prevented HFD-induced increment of bodyweight. The adipose tissue mass, liver enzymes, and plasma lipids were also reduced significantly (p<0.05) by the consumption of FCME. The mRNA expressions of adipogenic/lipogenic genes (PPARγ, C/EBPα, C/EBPβ, C/EBPγ, and SREBP-1C) in FCME-treated obese mice were considerably (p<0.05) suppressed. FCME showed its antiobesity potential by suppressing the body weight gain and by modulating the plasma lipids and liver enzymes through the regulation of adipogenic/lipogenic transcriptional factors. Fermented Cucurbita moschata could be an opportunistic agent in controlling obesity and fatty liver changes.

scholarly journals Gabra5LHA Mediate Astrocytic GABA-induced Obesity via Decreasing Energy Expenditure

2021 ◽  
Author(s):  
C. Justin Lee ◽  
Moonsun Sa ◽  
Eun-Seon Yoo ◽  
Wuhyun Koh ◽  
Mingu Gordon Park ◽  
...  
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Energy Expenditure ◽  
Mouse Model ◽  
Gene Silencing ◽  
Selective Inhibition ◽  
Hypothalamic Area ◽  
Adipose Tissues ◽  
Diet Induced Obesity ◽  
Distinct Subpopulation

The lateral hypothalamic area (LHA) regulates food intake and energy expenditure. Although LHA neurons innervate adipose tissues, the identity of neurons that regulate fat is undefined. Here we identify that Gabra5-positive neurons in LHA (Gabra5LHA) polysynaptically project to brown and white adipose tissues in the periphery. Gabra5LHA are a distinct subpopulation of GABAergic neurons and show decreased pacemaker firing in diet-induced obesity (DIO) mouse model. Gene silencing of Gabra5 in LHA decreases weight gain, whereas chemogenetic inhibition of LHA suppresses energy expenditure and increases weight gain. In DIO mouse model, Gabra5LHA are tonically inhibited by nearby reactive astrocytes releasing GABA, which is synthesized by MAOB. Administration of a MAOB inhibitor, KDS2010 reduces weight gain significantly without affecting food intake, which is recapitulated by gene-silencing of astrocytic MAOB in LHA. We propose that firing of Gabra5LHA facilitates energy expenditure and selective inhibition of astrocytic GABA is a molecular target for treating obesity.

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