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Insulin and obesity transform hypothalamic-pituitary-adrenal axis stemness and function in a hyperactive state.
Martin Werdermann1, Ilona Berger1, Laura D Scriba1
1Department of Internal Medicine III, University Hospital Carl Gustav Carus, Dresden University of Technology, Fetscherstraße 74, Dresden, 01307, Germany.
Molecular Metabolism
|November 6, 2020
Summary
Metabolic stress can prime progenitor cells in the brain-metabolic axis, leading to enhanced hormone production and a hyperactive hypothalamic-pituitary-adrenal axis. This early sensitization may increase the risk for metabolic syndrome later in life.
Area of Science:
- Endocrinology and Metabolism
- Neuroendocrinology
- Stem Cell Biology
Background:
- Metabolic diseases pose a growing societal challenge, with the brain-metabolic axis regulating homeostasis under stress.
- Metabolic inflammation and disease activate the hypothalamic-pituitary-adrenal axis, impacting overall physiological balance.
- Understanding the role of metabolic stress on progenitor cells within this axis is crucial for addressing metabolic disorders.
Purpose of the Study:
- To investigate the impact of metabolic stress on progenitor cells of the hypothalamic-pituitary-adrenal axis.
- To examine how hormones like insulin and leptin influence the proliferation and differentiation of pituitary and adrenal progenitor cells.
- To assess the effects of metabolic disease models on progenitor cells and hypothalamic-pituitary-adrenal axis activity.
Main Methods:
- In vitro studies applied insulin and leptin to murine pituitary and adrenal progenitor cells.
- In vivo studies utilized leptin-deficient (ob/ob) mice and high-fat diet-induced obesity models.
- Assessed progenitor cell proliferation, differentiation, hypothalamic-pituitary-adrenal axis activation, and gene expression (Npy, Agrp).
Main Results:
- Insulin significantly enhanced proliferation and differentiation of both pituitary and adrenocortical progenitor cells.
- No direct alterations in progenitor cells were observed in chronic metabolic stress models.
- Hyperactivation of the hypothalamic-pituitary-adrenal axis and altered appetite-regulating gene expression were noted in obese mice.
Conclusions:
- Early sensitization of hypothalamic-pituitary-adrenal axis progenitor cells by high insulin levels primes them for hyper-functional states and increased hormone production.
- Obese animals exhibit a hyperactive hypothalamic-pituitary-adrenal axis and adrenal hyperplasia, potentially explaining metabolic changes.
- This study suggests that early-life stress and metabolic alterations can sensitize progenitor cells, increasing the risk for developing metabolic syndrome in adulthood.
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