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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Key mediator of lipid-induced endoplasmic reticulum stress identified

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

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

Summary: "Impaired Nrf2 signaling causes significant decline in proteasomal activity and heightens ER stress response in lungs of patients with COPD and CS-exposed mice."

Malhotra, D., Thimmulappa, R., Vij, N., Navas-Acien, A., Sussan, T., Merali, S., Zhang, L., Kelsen, S. G., Myers, A., Wise, R., Tuder, R., and Biswal, S. (2009). Heightened endoplasmic reticulum stress in copd lungs: The role of nrf2-regulated proteasomal activity. American journal of respiratory and critical care medicine.

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

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Tonic Immobility in Childhood Sexual Abuse Survivors and Its Relationship to Posttraumatic Stress Symptomatology

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Loss of Nrf2 Signaling with ER Stress

We have explained that several factors can lead to impairment of Nrf2 including nutrition, actions of other proteins that interact with it, genetic factors, aging, endoplasmic reticulum stress, etc.  On the other hand, ER stress is characterized by the accumulation of misfolded proteins, altered Ca2+ regulation and up-regulations of other proteins including GRP78. Consistent activation of TRPV1, as well as, dopamine exposure has been known to lead to endoplasmic reticulum stress (Chen). This is a link to a slide presentation that was written by a co-worker of Tory Hagan's from Oregon State University about the Loss of Nrf2 signaling from ER stress.  We have cited Dr. Hagan's work before in other blogs in reference to Nrf2 and its decline in function from aging. (Fallahi)

Fallahi, A., Dixon, B., and Hagen, T. Loss of nrf2 dependant signaling following induction of endoplasmic reticulum stress. Visual Presentation, Oregon State University. http://www.citeulike.org/user/HEIRS/article/5730536
Chen, G. A. N. G., Bower, K. A., Ma, C., Fang, S., Thiele, C. J., and Luo, J. I. A. (2004). Glycogen synthase kinase 3beta (gsk3beta) mediates 6-hydroxydopamine-induced neuronal death. FASEB J., 18(10):1162-1164.  http://www.citeulike.org/user/HEIRS/article/5487100

TRPV1 and Endoplasmic Reticulum Stress

Activation of TRPV1 can cause endoplasmic reticulum stress which follows a pathway that leads to Nrf2 and unfolded protein response. Diabetes can lead to the unfolded protein response. In addition, chronic diabetic neuropathy can lead to nerve degeneration. DRG from diabetic rats show increased oxidative stress and cell injury. TRPV1 may be an early characteristic of diabetic sensory neuropathy.

• Note: Vitamin D has some preventative characteristics on endoplasmic reticulum stress.
  

Hong, S., Agresta, L., Guo, C., and Wiley, J. W. (2008). The trpv1 receptor is associated with preferential stress in large dorsal root ganglion neurons in early diabetic sensory neuropathy. Journal of Neurochemistry, 105(4):1212-1222.http://www.citeulike.org/user/HEIRS/article/2733060Civelek, M., Manduchi, E., Riley, R. J., Stoeckert, C. J., and Davies, P. F. (2009). Chronic endoplasmic reticulum stress activates unfolded protein response in arterial endothelium in regions of susceptibility to atherosclerosis. Circ Res, pages CIRCRESAHA.109.203711+. http://www.citeulike.org/user/HEIRS/article/5432618

Fibromyalgia, Endoplasmic Reticulum Stress, Neurotoxicity and CAMKII

Many experts now believe pain sensitivity in fibromyalgia is in part, neuropathic pain. "Martinez-Lavin notes that neuropathic pain is stimuli-independent and is accompanied by allodynia and paresthesia, which are also common features of fibromyalgia. He also points out that the most important characteristic of neuropathic pain is not the nerve lesion, but the resulting nerve dysfunction." (Kelly) Nociceptors (ie. TRPV1) can be upregulated in neuropathic conditions in addition to other inflammatory pain disorders. Also, a number of different agents activate nociceptors including those in food, fragrances and chemicals and other noxious stimuli like heat, cold and pH. Hormonals and neurochemical signals such as IGF and H2O2 and cytokines such as MCP-1 can increase the sensitivity of nociceptors which reduce their threshold for activation.
Upon activation of TRP channels, there is a flood of calcium inside the cell. Consistent and long-term activation and subsequent intracellular exposure to increased calcium may result in endoplasmic reticulum stress. Two consequences occur from ER stress 1) the activation of Nrf2 through PERK (Ho) which in endothelium includes Ho-1 binding to Nrf2 (Liu) and the 2) activation of CAMKII which may increase levels of cytokines and increase the likelihood of neuronal damage if not prevented. In cardiac cells, the inhibition of an isoform of CAMKII protects against intracellular levels of Ca+, H2O2 and acidosis in addition to protection from mitochondrial-induced apoptosis. Generally, H2O2 is generated through several mechanisms including from the mitochondrial respiratory chain and from activation of NADPH oxidases and can increase significantly during mitochondrial dysfunction. H2O2 signaling exerts prolonged signaling effects including those on dopamine release and down-regulation of CAMKII helps to prevent dopamine neurotoxicity(Cai, Bao). The activation of CAMKII from oxidative stress as noted by Xie, is responsible for "arrhythmia in diseased hearts and the heart's response to catecholamines in the "flight-fright" response (Cai). Also, CAMKII interacts with both TRPV1 and the NMDA receptor to alter their function. As for the latter, it may inhibit the downregulation of the NMDA receptor and increase the potential for pain generation and neurotoxicity.
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