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Participation of Arachidonic Acid and its Metabolites in Insulin Resistance (pp.133-160) $100.00
Authors:  (I. Pérez-Torres and G. Baños)
Metabolic syndrome (MS) is a cluster of metabolic abnormalities, which may
include obesity, insulin resistance (IR), hyperglycemia and hyperlipidemia. IR is a state
of impaired insulin activity in which normal insulin levels are incapable of producing the
corresponding normal insulin responses, and this state has been associated with supraphysiological
increases in glucose serum levels, causing a state of hyperglycemia. Human
and animal models with MS show altered arachidonic acid (AA) metabolism, resulting in
a shift from vasodilator prostaglandins (PGs) PGE1 to vasoconstrictor PGE2 metabolites,
originating from AA metabolism. AA is an ω-6 polyunsaturated fatty acid (PUFA), a
major component of mammalian cell membranes, and may account for up to 25 % of all
phospholipid (PL) fatty acids. It is released by phospholipases, from the PL bilayers of all
cell membranes (with the exception of those from red blood cells), in response to various
stimuli; it is subsequently metabolized through three different enzyme pathways, namely
cyclooxygenase (COX), lipoxygenase (LOX) and cytochrome (CYP) P450. AA may act
as a strong negative modulator of glucose uptake in pancreas, and it has been proposed
that there are higher serum levels of AA in diabetic subjects compared with normal
subjects. Other studies have shown a positive correlation between AA and insulin
sensitivity, although others, again, have shown a decrease in the AA concentration in MS
and obese children. The eicosanoids such as PGs, products of these pathways, can
participate in the development of IR, and PGE2 can increase insulin secretion through
interleukine (IL)-1β in pancreatic islets. These controversial differences can be partly
explained through the studies of enzyme pathways responsible for AA metabolism, as
well as its oxidation, elongation by Δ6-desaturase, or reintegration into the PL cell
membrane. It is the purpose of this chapter to show some of the relationships between
AA, its metabolism, the eicosanoids and IR. 

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Participation of Arachidonic Acid and its Metabolites in Insulin Resistance (pp.133-160)