Abstract
Obesity is reaching epidemic proportions and imposes major negative health crises and an economic burden in both high and low income countries. The multifaceted nature of obesity represents a major health challenge, with obesity affecting a variety of different organs and increases the risk of many other noncommunicable diseases, such as type 2 diabetes, fatty liver disease, dementia, cardiovascular diseases, and even cancer. The defining organ of obesity is the adipose tissue, highlighting the need to more comprehensively understand the development and biology of this tissue to understand the pathogenesis of obesity. Adipose tissue is a miscellaneous and highly plastic endocrine organ. It comes in many different sizes and shades and is distributed throughout many different locations in the body. Though its development begins prenatally, quite uniquely, it has the capacity for unlimited growth throughout adulthood. Adipose tissue is also a highly sexually dimorphic tissue, patterning men and women in different ways, which means the risks associated with obesity are also sexually dimorphic. Recent studies show that environmental factors during prenatal and early stages of postnatal development have the capacity to programme the structure and function of adipose tissue, with implications for the development of obesity. This review summarizes the evidence for a role for early environmental factors, such as maternal malnutrition, hypoxia, and exposure to excess hormones and endocrine disruptors during gestation in the programming of adipose tissue and obesity in the offspring. We will also discuss the complexity of studying adipose tissue biology and the importance of appreciating nuances in adipose tissue, such as sexual dimorphism and divergent responses to metabolic and endocrine stimuli. Given the rising levels of obesity worldwide, understanding how environmental conditions in early life affects adipose tissue phenotype and the subsequent development of obesity is of absolute importance.
Highlights
The increased incidence of obesity represents a major health challenge as it increases the risk of developing other noncommunicable diseases, including type 2 diabetes [2], fatty liver disease, [3], cardiovascular diseases [4], and cancer [5]
Understanding how environmental conditions in early life impact adipose tissue and the subsequent development of obesity is of absolute importance
There is some evidence to suggest that adipose tissue biology and obesity in female and male offspring may be differentially programmed by exposure to a maternal low protein diet during development [73, 81, 84] further work is required
Summary
Obesity is classed as a global epidemic by the World Health Organisation, with 13% of adults estimated to be obese in 2017 [1]. There is some evidence to suggest that adipose tissue biology and obesity in female and male offspring may be differentially programmed by exposure to a maternal low protein diet during development [73, 81, 84] further work is required. Animal studies of BPA and phalate exposure in utero have consistently shown to increase offspring adiposity in later life (Table 5 and [106, 110–112]) In part, these changes are associated with enhanced adipocyte size, infiltration of inflammatory leukocytes, and elevated expression of lipogenic markers, like PPAR-γ and SREBP [113]. Excess glucocorticoid exposure in utero was consistently shown to programme the offspring for increased adiposity (Table 6 and [119–123]) This was coupled with alterations in adipocyte morphology, expression of lipogenic genes, insulin signaling proteins and inflammatory cytokine expression in the offspring WAT [124]. Ad Lib ad libitum feeding, BAT brown adipose tissue, BPA bisphenol A, BW body weight, DEHP Di-2-ethylexyl phalate, GD gestational day, HFD high-fat diet, HFHS high fat high sugar diet, NA not applicable, SAT subcutaneous adipose tissue, VAT visceral adipose tissue, Vs versus, WAT white adipose tissue
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