Abstract
Stress is accompanied by metabolic alterations that could contribute to the etiology of diabetes mellitus, arteriosclerosis, and cardiovascular diseases; however, the mechanisms by which stress affects glucose and lipid metabolism remain to be resolved. Stress-induced effects on neurotransmission and interleukin-1 (IL-1) signaling rapidly produce hyperglycemia by increasing sympathetic outflow. Activation of the sympathetic nervous system can also rapidly stimulate lipolysis and hepatic triglyceride secretion. Furthermore, stress increases serum interleukin-6 (IL-6) and nerve growth factor (NGF) levels by activating neuroendocrine systems. IL-6 and NGF can rapidly increase lipolysis and hepatic triglyceride secretion without inducing hyperglycemia. The sympathetic nervous system does not mediate cytokine-induced hypertriglyceridemia. Thus, the central nervous system plays an important role in regulation of hepatic glucose and lipid metabolism via the sympathetic nervous system and cytokines.
Original language | English |
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Pages (from-to) | 192-197 |
Number of pages | 6 |
Journal | Trends in Endocrinology and Metabolism |
Volume | 8 |
Issue number | 5 |
DOIs | |
Publication status | Published - 1997 Jul |
Externally published | Yes |
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrinology