Objective(s): The molecular basis of “ metabolically healthy obese” and “ metabolically unhealthy nonobese” phenotypes is not fully understood. Our objective was to identify metabolite patterns differing in obese (metabolically healthy vs unhealthy (MHO vs MUHO)) and non-obese (metabolically healthy vs unhealthy (MHNO vs MUHNO)) individuals. Materials and Methods: This case-control study was performed on 86 subjects stratified into four groups using anthropometric and clinical measurements: MHO (21), MUHO (21), MHNO (22), and MUHNO (22). Serum metabolites were profiled using nuclear magnetic resonance (NMR). Multivariate analysis was applied to uncover discriminant metabolites, and enrichment analysis was performed to identify underlying pathways. Results: Significantly higher levels of glutamine, asparagine, alanine, L-glutathione reduced, 2-aminobutyrate, taurine, betaine, and choline, and lower level of D-sphingosine were observed in MHO group compared with MUHO. In comparison of MHNO and MUHNO groups, significantly lower levels of alanine, glycine, glutamine, histidine, L-glutathione reduced, and betaine, and higher levels of isoleucine, L-proline, cholic acid, and carnitine appeared in MUHNO individuals. Moreover, significantly affected pathways included amino acid metabolism, urea cycle and ammonia recycling in MUHO subjects and glutathione metabolism, amino acid metabolism, and ammonia recycling in MUHNO members. Conclusion: Literature review helped us to hint that altered levels of most metabolites might associate to insulin sensitivity and insulin resistance in MHO and MUHNO individuals, respectively. Besides, abnormal amino acid metabolism and ammonia recycling involved in unhealthy phenotypes (MUHO, MUHNO) might be associated with insulin resistance.

Background: Although a growing body of evidence suggests an association between obesity and depressive disorder, the association remains inconclusive. Metabolically healthy obese (MHO) phenotype, defined by favorable lipid profile, and normal insulin sensitivity, blood pressure, may be considered as a possible explanation for these inconsistencies. Accordingly, this study aimed to compare depression score among metabolic unhealthy obese (MUO) and age-and sex-matched healthy controls. Methods: In this comparative study including 157 Iranian adults, we assigned participants into three groups (non-obese metabolic healthy group, MHO and MUO) according to the BMI cutoff and MetS criteria. Depressive symptoms were assessed by Beck Depression Inventory. Analysis was done using SPSS version 14. 0. All variables are expressed as means± SD. One-way ANOVA and multiple linear regression were used for data analysis. Results: After adjustment for sex, marital status and educational level, MUO participants had significantly higher Beck depression score (p= 0. 036) compared to MHO and non-obese metabolic healthy groups. After adjustment for demographic variables, there was a significant association between waist circumference (β = 0. 142, p=0. 023), BMI (β = 0. 347, p= 0. 037), FBS (β = 0. 096, p< 0. 001), and the number of MetS components (β = 1. 71, p= 0. 002) with depression score. Conclusion: MHO was a benign phenotype in relation to depression.

Background: The prevalence of obesity is increasing worldwide. Obesity is associated with severe health effects. Abdominal obesity has a strong association with metabolic dysfunction. A subgroup of people with central obesity has been identified without typical metabolic disorders associated with obesity that has been known metabolically healthy abdominal obese (MHAO). The purpose of this review is to evaluate the MHAO phenotype in the context of type 2 DM incidence, risk of cardiovascular diseases, and all‑, cause of mortality. Methods: This is a protocol of systematic review. We will search PubMed/MEDLINE, EMBASE, Web of Science, Cochrane Library, and ProQuest. Additional studies will be identified through manual searching of reference lists. Quantitative studies evaluating abdominal obesity phenotype outcomes in adults will be included. Primary results will be assaying abdominal obesity phenotype results, including DM2 incidence, cardiovascular disease risk, and all‑, cause mortality. Two reviewers will independently screen full‑, text articles and abstract data. Statistical Analysis Used: Potential conflicts will be resolved through discussion. Results: The study methodological quality (or bias) will be appraised using appropriate tools. If feasible, we will conduct a random‑, effects meta‑, analysis. The researchers will also assess the quality of the articles independently based on Newcastle‑, Ottawa scale. Conclusions: The results of this review will provide a useful reference for the effect of abdominal obesity on metabolic dysfunction and cardiovascular or all‑, cause mortality.