Clinical Science (2008) 114, 183-193 - C.M. Aguilera and others - Alterations in plasma and tissue lipids associated with obesity and metabolic syndrome

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Clinical Science (2008) 114, (183–193) (Printed in Great Britain)

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Review article

Alterations in plasma and tissue lipids associated with obesity and metabolic syndrome

Concepción M. AGUILERA*, Mercedes GIL-CAMPOS†, Ramón CAÑETE† and Ángel GIL*

*Department of Biochemistry and Molecular Biology II, Institute of Nutrition and Food Technology, School of Pharmacy, University of Granada, Campus de Cartuja 18071 Granada, Spain, and †Unit of Pediatric Endocrinology, Reina Sofia University Hospital, Avda Menéndez Pidal s/n, Córdoba, Spain

Key words: AMP-dependent kinase (AMPK), fatty acid oxidation, hypothalamus, lipid, metabolic syndrome, non-esterified fatty acid (NEFA), obesity.

Abbreviations: ACC, acetyl-CoA carboxylase; AgRP, agouti protein; AMPK, AMP-activated protein kinase; apo, apolipoprotein; CE, cholesterol ester; CETP, CE transfer protein; CPT-1, carnitine-palmitoyl transferase-1; D6D, D⁶ desaturase; FA, fatty acid; FAS, FA synthase; HDL, high-density lipoprotein; HDL-C, HDL cholesterol; HL, hepatic lipase; HSL, hormone-sensitive lipase; IR, insulin resistance; LC-CoA, long-chain acyl-CoA; LCFA, long-chain FA; LDL, low-density lipoprotein; LPL, lipoprotein lipase; MS, metabolic syndrome; MUFA, monounsaturated FA; NEFA, non-esterified FA; NPY, neuropeptide Y; PI3K, phosphoinositide 3-kinase; PL, phospholipid; PPAR, peroxisome-proliferator-activated receptor; PUFA, polyunsaturated FA; SFA, saturated FA; TAG, triacylglycerol; Tri-C, triacsin C; VLDL, very-LDL.

The MS (metabolic syndrome) is a cluster of clinical and biochemical abnormalities characterized by central obesity, dyslipidaemia [hypertriglyceridaemia and decreased HDL-C (high-density lipoprotein cholesterol)], glucose intolerance and hypertension. Insulin resistance, hyperleptinaemia and low plasma levels of adiponectin are also widely related to features of the MS. This review focuses on lipid metabolism alterations associated with the MS, paying special attention to changes in plasma lipids and cellular fatty acid oxidation. Lipid metabolism alterations in liver and peripheral tissues are addressed, with particular reference to adipose and muscle tissues, and the mechanisms by which some adipokines, namely leptin and adiponectin, mediate the regulation of fatty acid oxidation in those tissues. Activation of the AMPK (AMP-dependent kinase) pathway, together with a subsequent increase in fatty acid oxidation, appear to constitute the main mechanism of action of these hormones in the regulation of lipid metabolism. Decreased activation of AMPK appears to have a role in the development of features of the MS. In addition, alteration of AMPK signalling in the hypothalamus, which may function as a sensor of nutrient availability, integrating multiple nutritional and hormonal signals, may have a key role in the appearance of the MS.