Abstract
The pandemic of type 2 diabetes mellitus (T2DM) has been largely attributed to the increasing prevalence of worldwide obesity at a geometric rate. However, the number of non-obese patients with T2DM is also on the rise, and it is as high as 60-80% in some Asian countries. These non-obese individuals have certain peculiarities and have a higher mortality rate compared with obese individuals. The pathophysiology of T2DM in non-obese individuals remains poorly understood, and this has an impact on defining its management. This review discusses the current understanding of the pathophysiology of T2DM in non-obese individuals. The definition of T2DM in non-obese individuals remains controversial because of the limited clinical measurements, and the current definition of obesity using body mass index (BMI) is not very helpful as these individuals have BMIs of <25K g/m3, which is considered normal. Many authors have argued that the so-called non-obese people are actually metabolically obese; however, in terms of the measurements clinically available, they are non-obese. The simplistic understanding of the mechanism of the pathophysiology sees it in terms of the balance between insulin secretion and insulin resistance. The pathogenesis of insulin resistance in a lean patient has been proven to be the same as what is seen in an obese individual, but most studies confirm more severe functional insulin secretory defects in lean individuals compared to the obese phenotype. The mechanism underlying this form of T2DM is still poorly defined, and more research is required to understand the mechanism of sarcopenic obesity, which some studies have revealed.
Highlights
BackgroundDiabetes mellitus (DM) is a heterogeneous disease and lacks a precise definition
The pathogenesis of insulin resistance in a lean patient has been proven to be the same as what is seen in an obese individual, but most studies confirm more severe functional insulin secretory defects in lean individuals compared to the obese phenotype
The mechanism underlying this form of type 2 diabetes mellitus (T2DM) is still poorly defined, and more research is required to understand the mechanism of sarcopenic obesity, which some studies have revealed
Summary
Diabetes mellitus (DM) is a heterogeneous disease and lacks a precise definition. Emphasis on modifiable risk factors like smoking and alcohol abuse that may further accelerate beta-cell failure in lean individuals may prevent further progression of the disease [18] These patients are neither clinically nor pathophysiologically related to LADA. A study suggests that lean T2DM had a lower beta-cell function using homeostatic model assessment beta (HOMA-B), compared to obese patients, without any significant difference in insulin resistance [30]. The decreased insulin secretion is partly due to decreased beta-cell function mass seen in both lean and obese individuals and additional functional defects of pancreatic insulin secretion, leading to blindness and hyperglycemia, which is more marked in the non-obese group Another relatively known defect contributing to the impaired insulin secretion in T2DM is the reduced secretion of the gut incretin hormones. A study by Taniguchi et al has demonstrated that insulin resistance is independently associated with subcutaneous and visceral fat areas in non-obese Japanese T2DM patients [37]
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