The overlapping epidemics of obesity and type 2 diabetes have been considered as syndemic. As originally conceived, the term syn demic was introduced to bring ‘new perspectives on the interaction between co- existing disorders in specific communities and with biological, behavioural and social factors that influence the occurrence and consequences of the diseases’. Obesity and type 2 diabetes represent two types of adverse interaction clustering: a bio logical–biological interface and a biological–social interface (Figure 1). The former relates to common genetic and physiological factors that underlie both obesity and type 2 diabetes, while shared environmental factors include changes in nutrition, physical activity, and psychological health.

Fig1. Pathways linking the syndemic of obesity and type 2 diabetes. CVD, cardiovascular disease.

Heritability for both obesity and type 2 diabetes is estimated to be moderate to high at between 30% and 70%.

Genome- wide association studies have identified ~700 variants for obesity [36] and >400 for type 2 diabetes. There is little shared genetic aetiology, which only accounts for ~15–20% of known heritability. A report in 2015 listed 49 loci (33 new) associated with waist- to- hip ratio adjusted for BMI, and an additional 19 loci newly associated with related waist and hip circumference measures. Many observational studies have shown correlations of obesity (and fat distribution) with type 2 diabetes, but do not in themselves allow inferences. The causal relationship between obesity and type 2 diabetes has been investigated, and established, using Mendelian randomization techniques. A polygenic risk score, based on 93 single- nucleotide polymorphisms (SNP) related to obesity in 119 859 individuals in the UK Biobank, found a near twofold increased risk for type 2 diabetes for each increase in BMI of 4.83 kg/m2, findings replicated in a study of up to 213 556 individuals from 14 prospective studies and randomized trials and 4 consortia. Genetic susceptibility to type 2 diabetes is mediated both through effects on insulin- release and insulin sensitivity. Epigenetic effects, impairing β- cell function, are also well described and can be acquired in utero, or by exposure to lifestyle factors including inactivity and obesity.

Syndromic obesities are increasingly recognized and for many the genetic basis has been identified. Many of the 79 identified syndromes in which obesity is a feature (e.g. Prader- Willi, Bardet- Biedl, Alström syndromes) also include a high prevalence of type 2 diabetes. Monogenic obesities are increasingly recognized, especially in children presenting with severe early- onset obesity, often with other features such as learning disability (Table 1). The development of specific treatments for a small minority of such obesities, some of which may progress to adulthood undiagnosed, emphasizes the increasing need for genetic diagnosis.

Table1. Genetic obesity syndromes.

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مواضيع ذات صلة

Production of Steroid Hormones—An Introduction

Profile of Bodily Cholesterol

Classes of Steroids

Modulation of the intestinal microbiome can alter in insulin sensitivity

Pathophysiology of obesity and diabetes

Obesity: definitions and phenotypes

Homeostasis—Maintenance of A Nearly Constant Internal Environment

Extracellular Fluid —The “Internal Environment”

Formation of Bone

THE PERIOSTEUM

Fibrocartilage

Elastic Cartilage