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Insulin fatty acid oxidation affected

An insulin infusion should be considered for severe cases of calcium channel blocker toxicity." Case reports suggest that an intravenous bolus of regular insulin (0.5-1 units/kg) with 50 mL dextrose 50% (0.25 mg/kg for children) followed with a continuous infusion of regular insulin (0.5-1 units/kg per hour) may improve myocardial contractility. The effect of insulin is presently unclear, but it may improve myocardial metabolism that is adversely affected by calcium channel blocker overdoses, such as decreased cellular uptake of glucose and free fatty acids and a shift from fatty acid oxidation to carbohydrate metabolism. This insulin regimen is titrated to improvement in systolic blood pressure over 100 mm Hg and heart rate... [Pg.139]

Although the effects of insulin on postprandial metabolism are profound, other factors (e.g., substrate supply and allosteric effectors) also affect the rate and degree to which these processes occur. For example, elevated levels of fatty acids in blood promote lipogenesis in adipose tissue. Regulation by several allosteric effectors further ensures that competing pathways do not occur simultaneously for example, in many cell types fatty acid synthesis is promoted by citrate (an activator of acetyl-CoA carboxylase), whereas fatty acid oxidation is depressed by malonyl-CoA (an inhibitor of carnitine acyltransferase I activity). The control of fatty acid metabolism is described in Section 12.1. [Pg.542]

Ultimately, dietary fatty acids seem to influence insulin sensitivity not only by altering cell membrane lipid composition, but also by affecting fatty acid oxidation and synthesis. The transcription factors involved with the ability of n-3 PUFAs to improve adiposity and insulin sensitivity, namely by PPARa and SREBP-1, may also work to improve adipocyte function, inflammation and insulin signalling. However, more research is needed to determine if OA and ALA can have the same effect on membrane PL composition and the transcription of genes involved in fatty acid synthesis and oxidation as the longer chain marine n-3 PUFAs. [Pg.268]

The fate of fatty acids entering the liver is markedly influenced by the ratio of insulin to glucagon in the circulation. High ratios favour esterification of fatty acids into acylglycerols and a low rate of )8-oxidation. Phospholipid biosynthesis is far less affected than that of triacylglycerols. The activity of PAP, however, is probably not directly dependent on insulin since it is increased in diabetes and starvation, both conditions where circulating insulin concentrations are low. [Pg.155]


See other pages where Insulin fatty acid oxidation affected is mentioned: [Pg.168]    [Pg.231]    [Pg.177]    [Pg.302]    [Pg.201]    [Pg.205]    [Pg.215]    [Pg.86]    [Pg.200]    [Pg.25]    [Pg.360]    [Pg.165]    [Pg.166]    [Pg.105]    [Pg.243]    [Pg.168]    [Pg.145]    [Pg.109]    [Pg.213]    [Pg.300]   
See also in sourсe #XX -- [ Pg.137 , Pg.260 ]




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