Insulin lipid mobilization

See also Adipocytes, Fat Absorption and Transport, Bile Salts and Emulsion of Fats, Mobilization of Stored Fat, Energy Storage, Triacylglycerol Synthesis, Action of Insulin, Lipids... 

Second-hit hypothesis This hypothesis has been proposed as a plausible explanation for the occurrence of NASH. (48, 70) The first hit is considered to be the development offatty liver, particularly due to hyperahmentation and obesity resulting in insulin resistance. As second hit follows the mobilization of free fatty acids from fat depots and their transport to the liver cells. This leads to a massive increase of free radicals due to oxidative stress with lipid peroxidation and induction of cytokines (TNFa, TGFp, IL6, IL8). As a result, there is a reactive formation of uncoupling protein (UCP2) with a subsequent decrease in hepatocyte ATP and a disturbance of macrophage function with higher sensitivity to endotoxin. This leads to an inflammatory reaction, cell death and the formation of fibrosis. (44, 50, 65)... 

C. Toxicity Cardiovascular adverse effects, which are extensions of the beta blockade induced by these agents, include bradycardia, atrioventricular blockade, and congestive heart failure. Patients with airway disease may suffer severe asthma attacks. Premonitory symptoms of hypoglycemia from insulin overdosage, eg, tachycardia, tremor, and anxiety, may be masked, and mobilization of glucose from the liver may be impaired. CNS adverse effects include sedation, fatigue, and sleep alterations. Atenolol, nadolol, and several other less lipid-soluble beta-blockers are claimed to have less marked CNS action because they do not enter the CNS as readily as other members of this group. 

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