scholarly journals Brown fat tissue: Therapeutic potential for insulin resistance, new hopes for tomorrow

2020 ◽  
Vol 4 (1) ◽  
pp. 022-023
Author(s):  
Seyedrafie Arefhosseini ◽  
Sepideh Alijani
Keyword(s):  
Insulin Resistance ◽  
Therapeutic Potential ◽  
Brown Fat ◽  
Fat Tissue

Therapeutic potential of curcumin in non-alcoholic steatohepatitis

2005 ◽  
Vol 18 (2) ◽  
pp. 212-221 ◽  
Author(s):  
Haim Shapiro ◽  
Rafael Bruck
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Animal Studies ◽  
Cell Activation ◽  
Therapeutic Potential ◽  
Stellate Cell ◽  
Indirect Evidence ◽  
Deficient Diet ◽  
Alcoholic Steatohepatitis ◽  
Ppar Γ

Non-alcoholic steatohepatitis (NASH) may be associated with a number of clinical conditions, but it occurs most commonly in patients with insulin resistance. There is as yet no established disease-modifying treatment, and a safe and broadly available agent that targets hepatic steatosis, insulin resistance, inflammation and fibrosis is necessary. The polyphenolic compound curcumin exhibits antioxidant and anti-inflammatory properties, inhibits NF-κB and activates PPAR-γ. In rodents, curcumin prevents dietary-induced hepatic steatosis, hepatic stellate cell activation and production of fibrotic proteins, and ameliorates steatohepatitis induced by the intake of alcohol or a methionine–choline-deficient diet. Indirect evidence suggests that curcumin may improve insulin sensitivity in diabetes and inflammatory states. The present paper reviews the numerous cellular and animal studies indicating that curcumin attenuates many of the pathophysiological processes involved in the development and progression of NASH. It is suggested that basic and clinical studies on curcumin in the development and progression of NASH are indicated.

Anti-obesity effect of taurine through inhibition of adipogenesis in white fat tissue but not in brown fat tissue in a high-fat diet-induced obese mouse model

Amino Acids ◽  
2018 ◽  
Vol 51 (2) ◽  
pp. 245-254 ◽  
Author(s):  
Kyoung Soo Kim ◽  
Min Ju Jang ◽  
Sungsoon Fang ◽  
Seul Gi Yoon ◽  
Il Yong Kim ◽  
...  
Keyword(s):  
Mouse Model ◽  
High Fat Diet ◽  
Brown Fat ◽  
Obese Mouse ◽  
Fat Tissue ◽  
High Fat ◽  
White Fat

scholarly journals Nutraceutical prospective: The synergetic mechanism of action of inositols and resveratrol on metabolic syndrome

2018 ◽  
Vol 2 (1) ◽  
pp. 35-38
Author(s):  
Antonio Malvasi ◽  
Andrea Tinelli ◽  
Domenico Baldini ◽  
Rossana G. Iannitti ◽  
Bernard Fioretti
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Therapeutic Potential ◽  
Second Messengers ◽  
Polycystic Ovarian Disease ◽  
Positive Effects ◽  
Medical Effectiveness ◽  
Synergistic Mechanism ◽  
Insulin Dependent ◽  
Dependent Processes

Abstract It has been known that inositols function as insulin second messengers and mediate different insulin-dependent processes and are a valid natural, non-pharmaceutical alternative to contrast insulin-resistance as well as associated metabolic syndrome in women with Polycystic ovarian disease (PCOS). Several studies also have shown positive effects of resveratrol in reducing glucose and lipid concentrations in patients. Recently, clinical evidence has proven that an D-chiro-inositol/resveratrol combination has a potential role to play in maintaining metabolic and endocrine health, however no large clinical trials have demonstrated the medical effectiveness of the combination, and the combined mode of action remains poorly discussed. Herein, we address the hypothesis of a synergistic mechanism adopted by D-chiro-inositol and resveratrol in reducing insulin resistance and hyperlipidemia and thus showing a greater therapeutic potential compared to treatment with inositol’s alone.

scholarly journals Type2Diabetes—Effect of Compensatory Oversecretion as a Reason forβ-Cell Collapse

2002 ◽  
Vol 3 (3) ◽  
pp. 153-158 ◽  
Author(s):  
Valdemar Grill ◽  
Anneli Björklund
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Clinical Studies ◽  
Structural Damage ◽  
Therapeutic Potential ◽  
Cell Collapse

Insulin secretion declines progressively before and during the course of type 2 diabetes. Evidence indicates that this process is, in part, secondary to increased requirement for insulin secretion that is brought about by insulin resistance and by hyperglycemia. The effects of over-secretion extend far beyond a mere reduction of available insulin stores and may cause not only functional but also structural damage. The time is ripe for clinical studies, which explore the therapeutic potential of reducing over-secretion.

The development of insulin resistance in brown adipose tissue may impair the acute cold-induced activation of thermogenesis in genetically obese (ob/ob) mice

1984 ◽  
Vol 4 (11) ◽  
pp. 933-940 ◽  
Author(s):  
Stewart W. Mercer ◽  
Paul Trayhurn
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Brown Fat ◽  
Acute Cold Exposure ◽  
Brown Adipose

Genetically obese (ob/ob) mice develop insulin resistance in brown adipose tissue during the fifth week of life. Prior to this, at 26 days of age, oh/oh mice show a substantial increase in GDP binding to brownadipose-tissue mitochondria during acute cold exposure. When insulin resistance in brown fat develops, by 35 days of age, the increase in GDP binding in response to cold is markedly reduced. Studies with 2-deoxyglucose suggest that insulin resistance in brown adipose tissue could impair thermogenic responsiveness during acute cold exposure by limiting the ability of the tissue to take up glucose.

Cytoplasmic p16 Is Expressed in Normal Brown Fat and Hibernomas

2020 ◽  
Vol 28 (5) ◽  
pp. 496-501
Author(s):  
Georgia Karpathiou ◽  
Jean Marc Dumollard ◽  
Zoe Evangelou ◽  
Anna Batistatou ◽  
Michel Peoc’h ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Brown Fat ◽  
Fat Tissue ◽  
P16 Expression ◽  
Tissue Browning

White adipose tissue browning has emerged as a putative therapy of obesity, and studies in mice have shown that Cdkn2a is implicated in white-to-brown transition. However, the role of Cdkn2a product p16 has been never studied in human brown fat tissue. The aim of the study is to investigate the expression of p16 in normal brown fat and in hibernoma, a lipoma containing brown fat-like adipocytes. Ten normal brown fat tissues and 5 hibernomas were immunohistochemically studied for p16 expression. Nearby white adipose tissue was used for comparison. All brown fat and hibernomas specimens express p16 in a cytoplasmic manner. Neighboring white adipose tissue is negative for p16 expression. Thus, cytoplasmic p16 may be associated with fat tissue browning.

scholarly journals GPR17 gene disruption does not alter food intake or glucose homeostasis in mice

2015 ◽  
Vol 112 (6) ◽  
pp. 1845-1849 ◽  
Author(s):  
Jason Mastaitis ◽  
Soo Min ◽  
Ralf Elvert ◽  
Aimo Kannt ◽  
Yurong Xin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Food Intake ◽  
Glucose Homeostasis ◽  
Gene Disruption ◽  
Therapeutic Potential ◽  
Intracerebroventricular Injection ◽  
Wild Type ◽  
Pharmacological Modulation ◽  
G Protein Coupled

G protein-coupled receptor 17 (GPR17) was recently reported to be a Foxo1 target in agouti-related peptide (AGRP) neurons. Intracerebroventricular injection of GPR17 agonists induced food intake, whereas administration of an antagonist to the receptor reduced feeding. These data lead to the conclusion that pharmacological modulation of GPR17 has therapeutic potential to treat obesity. Here we report that mice deficient in Gpr17 (Gpr17−/−) have similar food intake and body weight compared with their wild-type littermates. Gpr17−/− mice have normal hypothalamic Agrp mRNA expression, AGRP plasma levels, and metabolic rate. GPR17 deficiency in mice did not affect glucose homeostasis or prevent fat-induced insulin resistance. These data do not support a role for GPR17 in the control of food intake, body weight, or glycemic control.

Cardioprotective and antihypertensive effects of Enicostemma littorale Blume extract in fructose-fed rats

2012 ◽  
Vol 90 (8) ◽  
pp. 1065-1073 ◽  
Author(s):  
Niraj M. Bhatt ◽  
Meenal Chavda ◽  
Dipali Desai ◽  
Rishit Zalawadia ◽  
Vaibhav B. Patel ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vascular Reactivity ◽  
Therapeutic Potential ◽  
Serum Levels ◽  
Cardiovascular Complications ◽  
Oral Glucose ◽  
Protective Effects ◽  
High Fructose ◽  
Enicostemma Littorale ◽  
High Level

We investigated the protective effects of Enicostemma littorale Blume (EL) extract on hypertension and insulin resistance along with its associated cardiovascular complications in high fructose (HF) fed rats. For this, rats were divided among 4 groups: (i) control, fed laboratory chow; (ii) fed with a high level of fructose; (iii) fed with a high level of fructose plus E. littorale extract; and (iv) fed with a high level of fructose plus rosiglitazone (Rg). EL and Rg treatments were given simultaneously with HF diet. The results show that untreated HF-fed rats showed altered oral glucose tolerance, increased fasting insulin, and increased fasting glucose. These rats also exhibited hypertriglyceridemia, moderate hypertension, platelet hyperaggregability, decreased prothrombin time, activated partial thromboplastin time, altered vascular reactivity, and increased serum levels of enzymes (creatine kinase, type muscle–brain (CK-MB), aspartate aminotransferase (SGOT), lactate dehydrogenase (LDH), and alanine aminotransferase (SGPT). This is the first demonstration of platelet hyperaggregation and prothrombotic alteration in HF-fed rats. HF-fed rats treated with EL showed improved insulin resistance, along with reduced hypertriglyceridemia, hypertension, platelet aggregability, blood coagulation, serum enzymes (CK-MB, SGOT, LDH and SGPT), and vascular reactivity. These effects of EL in HF-induced hypertensive rats might be associated with the suppression of hyperinsulinemia and hypertriglyceridemia, along with its antiatherogenic and antithrombogenic potential. These data indicate that the aqueous extract of EL has great therapeutic potential for the prevention and (or) management of insulin resistance and the associated hypertension.

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