Mechanisms and Metabolic Implications of Regional Differences among Fat Depots
By T. Tchkonia, Thomas Thomou, Yi Zhu, Iordanes Karagiannides, C. Pothoulakis, M. Jensen, J. Kirkland. Cell Metabolism, 2013
648 citations recorded by the source corpus.
Fat distribution is closely linked to metabolic disease risk. Distribution varies with sex, genetic background, disease state, certain drugs and hormones, development, and aging. Preadipocyte replication and differentiation, developmental gene expression, susceptibility to apoptosis and cellular senescence, vascularity, inflammatory cell infiltration, and adipokine secretion vary among depots, as do fatty-acid handling and mechanisms of enlargement with positive-energy and loss with negative-energy balance. How interdepot differences in these molecular, cellular, and pathophysiological properties are related is incompletely understood. Whether fat redistribution causes metabolic disease or whether it is a marker of underlying processes that are primarily responsible is an open question.
Subfields: Epidemiology, Nutrition and Dietetics, Physiology
View Paper: https://www.semanticscholar.org/paper/1b51bc06b8ace473638da8e8aa242203eb26bc9f
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Citations in the corpus
- Obesity and type 2 diabetes mellitus: connections in epidemiology, pathogenesis, and treatments (2023, background): “the liver leads to steatosis, exacerbating insulin resistance by causing lipotoxicity-induced cellular dysfunction and apoptosis (40).”
- What We Talk About When We Talk About Fat (2014, positive): “Regardless of these distinctions, there are clearly important regional differences in such aspects of adipocyte behavior as adipokine secretion and rates of lipolysis and triglyceride synthesis (Tchkonia et al., 2013).”