Abstract
ObjectiveThe susceptibility to abdominal obesity and the metabolic syndrome is determined to a substantial extent during childhood and adolescence, when key adipose tissue characteristics are established. Although the general impact of postnatal nutrition is well known, it is not clear how specific dietary components drive adipose tissue growth and how this relates to the risk of metabolic dysfunction in adulthood. MethodsAdipose tissue growth including cell proliferation was analyzed in juvenile mice upon dietary manipulation with in vivo nucleotide labeling. The proliferative response of progenitors to specific fatty acids was assayed in primary cultures. Long-term metabolic consequences were assessed through transient dietary manipulation post-weaning with a second obesogenic challenge in adulthood. ResultsDietary lipids stimulated adipose tissue progenitor cell proliferation in juvenile mice independently of excess caloric intake and calorie-dependent adipocyte hypertrophy. Excess calories increased mitogenic IGF-1 levels systemically, whereas palmitoleic acid was able to enhance the sensitivity of progenitors to IGF-1, resulting in synergistic stimulation of proliferation. Early transient consumption of excess lipids promoted hyperplastic adipose tissue expansion in response to a second dietary challenge in adulthood and this correlated with abdominal obesity and hyperinsulinemia. ConclusionsDietary lipids and calories differentially and synergistically drive adipose tissue proliferative growth and the programming of the metabolic syndrome in childhood.
Highlights
The quantity, anatomical distribution, and functionality of adipose tissue as a lipid storing and endocrine organ are defining features and key drivers of the metabolic syndrome [1e4]
Dietary lipids accelerate juvenile adipose tissue progenitor proliferation independent of excess calories and adipocyte hypertrophy In order to determine the differential contribution of high dietary fat and excess calorie consumption to early post-lactation adipose tissue growth, we employed a pair-feeding approach by feeding female mice either a high-fat diet (HFD) ad libitum or a high fat and calorie content (HFD) load calorically matched (R-HFD) to the consumption of a group of mice on control diet (CD) (Figure S1A)
After 7 days of feeding, HFD mice showed significantly higher depot mass in intra-abdominal gonadal and subcutaneous fat, which was due to adipocyte hypertrophy with no change in the total adipocyte number, whereas R-HFD mice did not show any fat accumulation or adipocyte hypertrophy (Figure 1AeD)
Summary
The quantity, anatomical distribution, and functionality of adipose tissue as a lipid storing and endocrine organ are defining features and key drivers of the metabolic syndrome [1e4]. The contribution of excess calorie intake, dietary fat, and other nutritional factors is currently unclear [11e13] It is not known how components of early nutrition promote stable changes in the adipose tissue cellular composition thereby programming long-term tissue function, fat distribution, and systemic metabolism in adulthood. Systemic nutrient excess promotes lipid storage in adipocytes and adipocyte hypertrophy, resulting in enlargement of the fat depot, a reversible process contributing to obesity in young and adult age [14e16]. Both childhood and adult obesity are characterized by higher quantity of adipocytes (hyperplasia), representing a temporally more stable property [16e18]. Adipocytes are generated by the differentiation of resident immature adipocyte
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