Intrauterine Programming of Diabetes and Adiposity.
The prevalence of diabetes and adiposity has increased at an alarming rate and together they contribute to the rise in morbidity and mortality worldwide. Genetic studies till date have succeeded in explaining only a proportion of heritability, while a major component remains unexplained. Early life determinants of future risk of these diseases are likely contributors to the missing heritability and thus have a significant potential in disease prevention. Epidemiological and animal studies show the importance of intrauterine and early postnatal environment in programming of the fetus to adverse metabolic outcomes and support the notion of Developmental Origins of Health and Disease (DOHaD). Emerging evidence highlights the role of epigenetic mechanisms in mediating effects of environmental exposures, which in certain instances may exhibit intergenerational transmission even in the absence of exposure. In this article, we will discuss the complexity of diabetes and increased adiposity and mechanisms of programming of these adverse metabolic conditions.
CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB), Hyderabad, 500 007, India.
Ashutosh Singh
AS
Tomar
CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB), Hyderabad, 500 007, India.
Divya Sri Priyanka
DS
Tallapragada
CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB), Hyderabad, 500 007, India.
Suraj Singh
SS
Nongmaithem
CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB), Hyderabad, 500 007, India.
Smeeta
S
Shrestha
Diabetes Unit, King Edward Memorial Hospital and Research Centre, Pune, India.
Chittaranjan S
CS
Yajnik
CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB), Hyderabad, 500 007, India. chandakgrc@ccmb.res.in.|Adjunct Group Leader, Genome Institute of Singapore, Singapore, Singapore. chandakgrc@ccmb.res.in.
Giriraj Ratan
GR
Chandak
D050154:Adiposity / Q000235:genetics*; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology / Q000235:genetics*; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000235:genetics*; D044127:Epigenesis, Genetic; D005260:Female; D047109:Fetal Development / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D006801:Humans; D007333:Insulin Resistance; D039382:Maternal Nutritional Physiological Phenomena; D009765:Obesity / Q000150:complications / Q000235:genetics*; D015995:Prevalence
Diabesity; Fetal programming; Fuel- and nutrient-mediated teratogenesis; Intermediate traits; Mendelian randomization; Thrifty epigenotype