Dietary calories and lipids synergistically shape adipose tissue cellularity during postnatal growth
| Autor: | Sarah Lerch, Irina Meln, Johanna Koddebusch, Gretchen Wolff, Thomas Gajek, Liza Harbrecht, Hellmut G. Augustin, Alexandros Vegiopoulos, Irem Bayindir-Buchhalter, Damir Krunic, Wujun Hong |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty lcsh:Internal medicine Pediatric Obesity Abdominal Fat Adipose tissue 030209 endocrinology & metabolism Nutrient sensing Biology Programming of disease Brief Communication 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Internal medicine medicine Hyperinsulinemia Adipocytes Palmitoleic acid Animals Childhood obesity Progenitor cell Insulin-Like Growth Factor I lcsh:RC31-1245 Molecular Biology Abdominal obesity Cells Cultured Cell Proliferation Cell Biology medicine.disease Lipid Metabolism Dietary Fats Metabolic syndrome Mice Inbred C57BL 030104 developmental biology Endocrinology chemistry Progenitor cell proliferation Female medicine.symptom Adipocyte hypertrophy Energy Intake |
| Zdroj: | Molecular Metabolism Molecular Metabolism, Vol 24, Iss, Pp 139-148 (2019) |
| ISSN: | 2212-8778 |
| Popis: | Objective The 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. Methods Adipose 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. Results Dietary 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. Conclusions Dietary lipids and calories differentially and synergistically drive adipose tissue proliferative growth and the programming of the metabolic syndrome in childhood. Highlights • Dietary fat accelerates adipose tissue progenitor proliferation in juvenile mice. • Lipid-mediated proliferation is independent of excess calorie intake. • Excess calories elevate IGF-1 levels and adipocyte hypertrophy. • Palmitoleic acid enhances the proliferative response of progenitors to IGF-1. • Lipids and calories in childhood program features of the adult metabolic syndrome. |
| Databáze: | OpenAIRE |
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