<p>Resting Whole Body Energy Metabolism in Class 3 Obesity; from Preserved Insulin Sensitivity to Overt Type 2 Diabetes</p>

Abstract

Context: Insulin resistance and diabetes may influence separately or in combination whole body energy metabolism. Objective: To assess the impact of insulin resistance and/or overt type 2 diabetes on resting energy expenditure (REE) in class 3 obese individuals. Design and Setting: Retrospective, cross-sectional analysis of a set of data about individuals attending the outpatients service of a single center of bariatric surgery between January 2015 and December 2017. Patients: We screened 382 patients in which abnormal thyroid function was excluded, and segregated them in three groups of subjects: patients with type 2 diabetes (T2DM; n=70), nondiabetic insulin-resistant patients with HOMA-IR ≥ 3 (n=236), non-diabetic insulin-sensitive patients with HOMA-IR < 3 (n=75). Main Outcome Measure: Resting energy expenditure (REE), body composition and insulin resistance assessed using indirect calorimetry, bioimpedance and HOMA-IR. Results: Non-diabetic insulin-sensitive patients resulted to be younger, with lower BMI and higher prevalence of female subjects; meanwhile, non-diabetic but insulin-resistant patients and T2DM patients were not different in terms of anthropometric parameters. REE was higher in T2DM than in non-diabetic insulin-resistant and insulin-sensitive individuals when expressed as percent of the predicted REE (based on Harris Benedict equation) (p<0.0001) or when adjusted for kg of free fat mass (p<0.0001) and was found to be higher also in insulinresistant vs insulin-sensitive patients (p<0.001). The respiratory quotient was different between groups (0.87±0.11, 0.86±0.12 and 0.91±0.14 in T2DM, insulin-resistant and insulinsensitive patients, respectively; p<0.03). Regression analysis confirmed that HOMA-IR was independently associated with the REE (R 2 =0.110, p<0.001). Conclusion: Class 3 obese patients with normal insulin sensitivity are characterized by reduced fasting REE in comparison to insulin-resistant obese patients and obese patients with short duration of diabetes supporting the hypothesis that down-regulation of nutrients' oxidative disposal may represent an adaptation of energy metabolism in obese individuals with preserved insulin sensitivity.

Correlation analysis of carotid plaque in young patients with newly diagnosed type 2 diabetes and platelet-to-lymphocyte ratio and neutrophil–lymphocyte ratio

“…Therefore, the overall risk of stroke and ischemic stroke has significantly increased. 29 A study found that the majority of young type 2 diabetes mellitus patients were obese, 30 and the increased IMT in young adults was associated with obesity. 31 Type 2 diabetes mellitus in youth becomes quickly aggressive after its onset, as the rate of functional impairment in the islet B cells occurs relatively quickly.…”

TG/HDL Ratio Is an Independent Predictor for Estimating Resting Energy Expenditure in Adults with Normal Weight, Overweight, and Obesity

“…The present data suggest that the impact of having a high body mass on REE becomes most influential when both body mass and insulin resistance are severely high. Baseline data from bariatric surgery patients with Class III obesity showed that those with insulin resistance had a higher REE than those who were insulin-sensitive, even when adjusted for fat-free mass [ 43 ]. Both the HOMA-IR score and TG/HDL ratio were significantly higher in participants with Class III obesity compared to those with Class I/II obesity.…”

<p>Inadequacy of Vitamin D Nutritional Status in Individuals with Metabolically Unhealthy Obesity Phenotype: The Relevance of Insulin Resistance</p>

“…The present study observed, in accordance with HOMA-IR criteria adopted to classify obesity phenotype, the prevalence of MUHO was higher than MHO in our population. Studies suggest that MUHO is characterized by a lower inflammatory cytokine environment than MHO [23][24][25] and the last phenotype may be caused by several mechanisms, 26 including preserved insulin sensitivity, specific fat distribution with low visceral and ectopic fat accumulation compared with subcutaneous fat depots, normal adipose tissue function defined by lower adipocyte size, less macrophage infiltration into adipose tissue, 27 and normal adipokine secretion. 26,28 However, more studies are necessary to identify the mechanisms that promote a healthy metabolic profile in individuals with obesity.…”