Contribution of markers of adiposopathy and adipose cell size in predicting insulin resistance markers in women of varying age and adiposity

Markers of adipose tissue (AT) dysfunctions, such as adipocyte hypertrophy, macrophage infiltration and secretory adiposopathy (low plasma adiponectin/leptin, A/L, ratio), associate with metabolic disorders. However, no study has compared the relative contribution of these markers to cardiometabolic risk in women of varying age and adiposity. Body composition, regional AT distribution, lipid-lipoprotein profile, glucose homeostasis and plasma A and L levels were determined in 67 women (age: 40-62 years; BMI: 17-41 kg/m2). Expression of macrophage infiltration marker CD68 and adipocyte size were measured from subcutaneous abdominal (SCABD) and omental (OME) fat samples. AT dysfunction markers were correlated with most lipid-lipoprotein levels such as TAGs (-0.36<rho<0.46; 0.0005<p<0.05), except OME CD68 expression which was negatively related to HDL-cholesterol. The A/L ratio was negatively associated with fasting insulinemia and HOMA-IR (-0.60<rho<-0.63; p<0.0001), while SCABD or OME adipocyte size and SCABD CD68 expression were positively related to these variables (0.39<rho<0.59; p<0.01). Multiple regression analyses including these markers and triacylglycerol (TAG) levels revealed that the A/L ratio was the only predictor of fasting insulinemia and HOMA-IR (partial R2=0.31-0.33; 0.000<p<0.005) in the model with TAGs and CD68 expression. However, the contribution of the A/L ratio was supplanted by adipose cell size in the model where the latter replaced TAGs. Combination of tertiles of largest adipocyte size and lowest A/L ratio showed the highest HOMA-IR. Taken together, our results show that adipocyte hypertrophy combined with reduced A/L ratio was related to increased IR, suggesting an independent contribution of both markers to the variance of cardiometabolic risk.

Multidimensional Single-Nuclei RNA-Seq Reconstruction of Adipose Tissue Reveals Adipocyte Plasticity Underlying Thermogenic Response

Adipose tissue has been classified based on its morphology and function as white, brown, or beige / brite. It plays an essential role as a regulator of systemic metabolism through paracrine and endocrine signals. Recently, multiple adipocyte subtypes have been revealed using RNA sequencing technology, going beyond simply defined morphology but by their cellular origin, adaptation to metabolic stress, and plasticity. Here, we performed an in-depth analysis of publicly available single-nuclei RNAseq from adipose tissue and utilized a workflow template to characterize adipocyte plasticity, heterogeneity, and secretome profiles. The reanalyzed dataset led to the identification of different subtypes of adipocytes including three subpopulations of thermogenic adipocytes and provided a characterization of distinct transcriptional profiles along the adipocyte trajectory under thermogenic challenges. This study provides a useful resource for further investigations regarding mechanisms related to adipocyte plasticity and trans-differentiation.HighlightsMultidimensional transcriptome analysis at single-nucleus resolution recovers nuclei of cell types in adipose tissueAdaptative thermogenic response results in 3 distinct mature adipose cell typesSingle-nuclei transcriptomic-based secretome analysis reveals adipose cell-type-specific genesThe in vivo trajectory of adipocyte plasticity for thermogenic response reveals sets of trans-differentiation genes

Analysis on Overweight and Inadequate Physical Activity by Nutritional Behaviors such as Obesity

We study all the review article related to Obesity. The Obesity is the disease in which imbalance between the calorie intake and its use. Obesity has touched widespread levels in established as well as in developing countries. It progressively existence experiential by altering the lifestyle of the family. The mechanism of Obesity is the unusual calorie convert into fat in adipose tissue. Adipose tissue consists of an adipose cell and unusual calorie accumulate into the adipose cell they swell increase their Weight and increase the bodyweight of the body. Universally in an investigation of 199 nations, 1.46 billion grown-ups are assessed to actuality overweight, and 502 million are assessed as existence stout. Individuals are commonly viewed as fat when their weight file (BMI) an estimation developed by segmentation an individual load by the rectangular of the separate tallness is more than 30 Kg/m2, by the reference range 25-30 kg/m2 considered as overweight. Weight Index (BMI) is commonplace uses to clarify the overweight and heftiness in the study of disease transmission contemplates. In any case, BMI has low affectability and there is bigger entomb singular changes in the percent muscle versus fat for some random BMI esteem, somewhat trait to age sex and nationality. Causes of Obesity, both genes and environmental factor participate in Obesity. However, by the large, genes are now thought to set only the stage and provide the background, against which the decisive effects and provide effects are eventually driven by the natural and conduct factors.

Adipose cell size changes are associated with a drastic actin remodeling

Adipose tissue plays a major role in regulating whole-body insulin sensitivity and energy metabolism. To accommodate surplus energy, the tissue rapidly expands by increasing adipose cell size (hypertrophy) and cell number (hyperplasia). Previous studies have shown that enlarged, hypertrophic adipocytes are less responsive to insulin, and that adipocyte size could serve as a predictor for the development of type 2 diabetes. In the present study, we demonstrate that changes in adipocyte size correlate with a drastic remodeling of the actin cytoskeleton. Expansion of primary adipocytes following 2 weeks of high-fat diet (HFD)-feeding in C57BL6/J mice was associated with a drastic increase in filamentous (F)-actin as assessed by fluorescence microscopy, increased Rho-kinase activity, and changed expression of actin-regulating proteins, favoring actin polymerization. At the same time, increased cell size was associated with impaired insulin response, while the interaction between the cytoskeletal scaffolding protein IQGAP1 and insulin receptor substrate (IRS)-1 remained intact. Reversed feeding from HFD to chow restored cell size, insulin response, expression of actin-regulatory proteins and decreased the amount of F-actin filaments. Together, we report a drastic cytoskeletal remodeling during adipocyte expansion, a process which could contribute to deteriorating adipocyte function.