ER Stress in Adipocytes Inhibits Insulin Signaling, Represses Lipolysis, and Alters the Secretion of Adipokines Without Inhibiting Glucose Transport

ER stress in adipocytes might initially lead to changes resembling early prediabetic stages, which at least in part support the regulation of systemic energy homeostasis.

HEIRS Research Tags: ER Stress
Library: Endoplasmic reticulum stress

CiteULike: ER Stress in Adipocytes Inhibits Insulin Signaling, Represses Lipolysis, and Alters the Secretion of Adipokines Without Inhibiting Glucose Transport: "Xu, L., Spinas, G. A., and Niessen, M. (2010). Er stress in adipocytes inhibits insulin signaling, represses lipolysis, and alters the secretion of adipokines without inhibiting glucose transport. Hormone and Metabolic Research."


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Heightened endoplasmic reticulum stress in copd lungs: The role of nrf2-regulated proteasomal activity.

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Calcium/calmodulin-dependent protein kinase II links ER stress with Fas and mitochondrial apoptosis pathways

Calcium/calmodulin-dependent protein kinase II links ER stress with Fas and mitochondrial apoptosis pathways.

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Prolonged stress sparks ER to release calcium stores and induce cell death in aging-related diseases

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Endoplasmic Reticulum Stress

PBDE (flame retardents), dioxins, PCBs etc bioaccumulate in fat tissue. One study shows that agents that cause ER stress result in failure of preadipocyte differentiation, failure to accumulate lipid, inhibit PPAR-gamma and adiponectin and resulted in sustained synthesis of MCP-1. (MCP-1 is associated with sickness syndrome.) Other agents that inhibited GATA during the study seemed to do the same. Suggesting that agents that cause ER stress may inhibit GATA and cause these changes. Adiponecting and PPAR-gamma are both anti-inflammatory regulators.

Shimada, T., Hiramatsu, N., Okamura, M., Hayakawa, K., Kasai, A., Yao, J., and Kitamura, M. (2007). Unexpected blockade of adipocyte differentiation by k-7174: Implication for endoplasmic reticulum stress. Biochemical and Biophysical Research Communications, 363(2):355-360. http://www.citeulike.org/user/HEIRS/article/5436816