The PPARGrs1801282 (G/C) polymorphism has been associated with OSA in obese Indian subjects, whereas no such association has been reported in Chinese Han subjects.
An involvement of FABP4 in the pathogenesis of obesity and insulin resistance seems to be mediated via FABP4-dependent peroxisome proliferator-activated receptor γ (PPARγ) inhibition.
These results conclude that the BGE extract containing several kinds of polymethoxy flavones showed PPARγ ligand-binding capacity in vitro and prevented obesity and insulin resistance independent of adiponectin secretion in mice.
VDR and PPARγ mRNA expression was higher in the adipose tissues of GDM women in comparison to that of women with normal glucose tolerance (VDR mRNA: G1 vs. N1: 210.00 [90.58-311.46] vs. 89.34 [63.74-159.92], G2 vs. N2: 298.67 [170.84-451.25] vs. 198.28 [119.46-261.23], PPARγ mRNA: G1 vs. N1: 100.72 [88.61-123.87] vs. 87.52 [66.37-100.04], G2 vs. N2: 117.33 [100.08-149.00] vs. 89.90 [76.95-109.09], P < 0.05), and their expression was the highest in GDM + overweight/obese women.
These findings indicate that HSPA12A is a novel regulator of adipocyte differentiation and diet-induced obesity through a positive feedback regulation with PPARγ.
These results suggest that the combined regulation of PPARγ, SMAD and the adrenergic receptor signalling pathway synergistically induces brown adipogenesis and may serve as an effective strategy to treat obesity and related diseases, including type 2 diabetes.
Obesity rats induced by 8-week high fat diet (HFD) were randomly divided into obesity group (OB) and exercised obesity group (EOB) with 8 rats each group, and 40 diabetes rats established by 8-week HFD plus low dose of streptozotocin were randomly divided into 4 groups: diabetes group (DM), exercised diabetes group (EDM), exercised diabetes plus PPARγ agonist pioglitazone group (EDP), and exercised diabetes plus PPARγ antagonist GW9662 group (EDG).
Here we dissected the specific role of high-fat-diet (HFD)-induced obesity and vascular smooth muscle cell (VSMC)-PPARγ for remodelling of small pulmonary arteries.
It was found that resistin expression is significantly correlated with lipid profile and inflammatory status in obesity and atherosclerotic groups, and PPARγ agonist administration significantly improves inflammatory status and dyslipidemic profile across studied groups (p < .05).
We further show that in the context of diet-induced obesityPPARγ-K107R-mutant mice have enhanced insulin sensitivity without the corresponding increase in adiposity that typically accompanies PPARγ activation by TZDs.
MiR-27a derived from these adipocytes induced insulin resistance in C2C12 skeletal muscle cells through miR-27a-mediated repression of PPARγ and its downstream genes involved in the development of obesity.
These results suggest that CD38 deficiency impairs adipogenesis and lipogenesis through activating Sirt1/PPARγ-FASN signalling pathway during the development of obesity.
Here, we show that targeted PPARγ mutations resulting in constitutive deacetylation (K268R/K293R, 2KR) increased energy expenditure and protected from visceral adiposity and diet-induced obesity by augmenting brown remodeling of white adipose tissues.
An interaction between ERRα and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) has also recently been shown to regulate an enzyme in the β-oxidation of free fatty acids, thereby suggesting that ERRα plays an important role in obesity and type 2 diabetes.
Peroxisome proliferator activated receptor-gamma (PPAR-γ) is implicated in several metabolic syndromes including Diabetic Nephropathy, besides obesity, insulin insensitivity, dislipidemia, inflammation, and hypertension.
Chitosan Oligosaccharides Improve Glucolipid Metabolism Disorder in Liver by Suppression of Obesity-Related Inflammation and Restoration of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ).