Insulin Resistance Assessment in Relation to Obesity Levels Among Iraqi Type 2 Diabetics View PDF
*Mohammad Abdul Ghafoor Mohammad
Medicine, Basrah Health Directorate, Al-Sayab Teaching Hospital, Al-Sayab Teaching Hospital, Basrah, Iraq
*Corresponding Author: Mohammad Abdul Ghafoor Mohammad
Medicine, Basrah Health Directorate, Al-Sayab Teaching Hospital, Al-Sayab Teaching Hospital, Basrah, Iraq
Published on: 2025-08-01
Abstract
Diabetes mellitus (DM) represents a metabolic syndrome characterized by dysregulation of carbohydrate metabolism. Obesity is recognized as a principal modifiable risk factor predisposing individuals to type 2 DM (T2DM) and is defined by excessive adiposity. In the obese state, adipose tissue exhibits increased secretion of non-esterified fatty acids, glycerol, hormonal mediators, pro-inflammatory cytokines, and additional bioactive substances that collectively contribute to the pathogenesis of insulin resistance (IR). A robust and well-documented association exists between body mass index (BMI), IR, and the subsequent development of T2DM. The present investigation aimed to elucidate the relationship between degrees of obesity and IR among Iraqi patients diagnosed with T2DM. Specifically, the study sought to quantify the impact of IR relative to obesity severity within this population group. A case-control study design was employed, encompassing 300 participants (163 females and 137 males), aged between 30 and 60 years, over the period extending from July to December 2024 study subjects, including both cases and controls, were stratified into four categories based on BMI: normal weight, overweight, obese, and markedly obese. All participants provided informed consent consistent with World Health Organization ethical guidelines. Biochemical and anthropometric assessments comprised the homeostatic model assessment of IR (HOMA-IR), glycated hemoglobin (HbA1c), fasting blood glucose (FBG), comprehensive lipid profile, and BMI determination. Comparative analysis demonstrated that the case group exhibited significantly elevated levels of FBG, HbA1c, total cholesterol, triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and HOMA-IR compared to the control group (p = 0.001). Conversely, no statistically significant difference was observed between groups regarding high-density lipoprotein cholesterol (HDL-C) concentrations. Emerging evidence underscores that incremental increases in BMI are associated with progressive reductions in insulin sensitivity and amplification of IR, ultimately facilitating the onset and progression of T2DM.
Keywords
Diabetes mellitus, Cholesterol, Triglycerides, Insulin resistance, Obesity
Introduction
T2DM is recognized as a chronic metabolic disorder that is fundamentally characterized by persistent hyperglycemia. This hyperglycemic state primarily arises due to an impaired responsiveness of insulin receptors to circulating insulin, a mechanism commonly referred to as IR [1]. In other words, IR represents a pathological condition in which normal physiological concentrations of insulin are insufficient to produce the expected biological responses. Specifically, this dysfunction manifests as an inadequate capacity of cells to uptake and utilize glucose effectively, alongside a failure to appropriately suppress circulating TG levels. It is important to highlight that the emergence and progression of IR results from a multifaceted interaction between inherent genetic factors and modifiable lifestyle components. Among these, dietary habits and a sedentary lifestyle, characterized by reduced physical activity, play a particularly significant role [2].
In the context of assessing obesity and its relationship to metabolic disturbances, BMI has emerged as a widely accepted and validated proxy indicator of body fatness. Notably, BMI offers a practical alternative to direct methods of body composition measurement. This is largely because the calculation of BMI is both precise and highly accessible, rendering it one of the most reliable approaches for evaluating overweight and obesity across diverse populations. Moreover, the simplicity and low cost of BMI estimation facilitate its widespread utilization by clinicians as well as the general public, given that only height and weight measurements are required [3].
Given this background, the present study was designed to explore the association between BMI and lipid profile parameters in Iraqi individuals diagnosed with T2DM. Understanding this relationship is crucial, as insulin performs essential regulatory functions within metabolic pathways. In particular, insulin inhibits lipolysis in adipose tissue and simultaneously promotes the activity of lipoprotein lipase, an enzyme that plays a central role in lipid metabolism. Furthermore, in the setting of obesity, the progressive expansion of adipose tissue contributes to the increased mobilization of free fatty acids (FFAs) into systemic circulation. This process occurs through the activation of hormone-sensitive lipase, an enzyme regulated by cyclic AMP-dependent signaling pathways. In addition to this mechanism, FFAs are also released within peripheral tissues as a result of lipoprotein lipase-mediated hydrolysis of TG-rich lipoproteins [4]. It is also worth noting that the prevalence of obesity, metabolic syndrome, and their associated metabolic derangements is shaped by a wide array of contributing factors. These include genetic susceptibility, age, sex, the quantity and composition of dietary intake, the degree of physical activity, and individual body habitus [5]. To objectively quantify IR in clinical and research settings, the HOMA-IR has been established as a reliable and widely used methodological tool for estimating β-cell function and the degree of IR [6].
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