Obesity reduces life expectancy, lowers quality of life, and causes numerous cardiometabolic diseases and some cancers. However, the individual risk of developing obesity-associated comorbidities is highly variable and cannot be explained only by body mass index. Observations that some obese people have a low risk for cardiometabolic disorders gave rise to the notion of metabolically healthy obesity (MHO). Despite the lack of a precise definition, MHO is typically identified by normal glucose and lipid metabolism indices, as well as the absence of hypertension. In individuals with MHO, the absence of metabolic abnormalities may minimize the risk of mortality, cardiovascular diseases, chronic kidney disease, dementia, and cancer, compared to metabolically unhealthy individuals with obesity. However, MHO appears to be a temporary phenotype that may not confer permanent benefits to individuals with obesity, further justifying therapeutic efforts to maintain metabolic fitness. In this review, we describe the traits of the MHO phenotype, its changeable nature, and the factors associated with phenotype change. In addition, we discuss the clinical outcomes of the MHO phenotype, particularly focusing on the transition of metabolic health over time and its effect on cardiometabolic disorders. Finally, the clinical importance of maintaining metabolic health is emphasized.
Nonalcoholic fatty liver disease (NAFLD), which has recently undergone a change in its definition and acronym to “metabolic dysfunction associated fatty liver disease (MAFLD),” is clinically significant as an increasingly prevalent independent risk factor for cardiovascular diseases. Insulin resistance is considered to be a key mechanism in the development and progression of NAFLD/MAFLD, and fatty liver disease itself may exacerbate insulin resistance. In this review, we describe the mechanisms underlying the interaction between insulin resistance and fatty liver, and we summarize the therapeutic attempts based on those mechanisms.
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Increased inflammation and insulin resistance are commonly observed in obesity and diabetes. Inflammatory mediators secreted by the adipose tissue contribute to the pathogenesis of diabetes and cardiovascular diseases. Free fatty acids and pro-inflammatory cytokines from adipose tissue inhibit the intracellular insulin signaling pathway, further contributing to the progression of diabetes. Meta-analysis studies show that high sensitivity C-reactive protein can be used as a predictor of future all-cause mortality, including cardiovascular and cancer mortality. In addition to the discovery of novel therapeutic methods targeting inflammatory mediators, basic lifestyle interventions, such as regular exercise, healthy eating, and proper weight control, are absolutely crucial for reducing inflammation and preventing mortality.
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The number of patients with type 2 diabetes (T2D) is increasing worldwide and that in Korea, particularly, has shown an exponential increase with a rise in the older population. The diabetic population is predicted to soar up to 6 million by 2050. The prevalence of diabetes among Korean adults is approximately 15%, while that of prediabetes is 25%, with a total prevalence of 40%. As 40% of the prediabetes cases subsequently progress to T2D, prevention through proactive interventions at the prediabetes stage is essential to reduce the socioeconomic burden due to T2D and the complications of diabetes. With regard to the prevention of T2D, new findings have been published related to the implementation of lifestyle interventions such as exercise and diet as well as drug treatments and surgeries, which have deepened our understanding of the prevention of T2D. Based on published evidence, this review aimed to examine the methods used in the prevention of diabetes.