Abstract
BackgroundThe metabolic syndrome, known also as the insulin resistance syndrome, refers to the clustering of several risk factors for atherosclerotic cardiovascular disease. Dyslipidaemia is a hallmark of the syndrome and is associated with a whole body reduction in the activity of lipoprotein lipase (LPL), an enzyme under the regulation of the class of nuclear receptors known as peroxisome proliferator-activated receptor (PPAR). Glycyrrhizic acid (GA), a triterpenoid saponin, is the primary bioactive constituent of the roots of the shrub Glycyrrhiza glabra. Studies have indicated that triterpenoids could act as PPAR agonists and GA is therefore postulated to restore LPL expression in the insulin resistant state.ResultsOral administration of 100 mg/kg of GA to high-fat diet-induced obese rats for 28 days led to significant reduction in blood glucose concentration and improvement in insulin sensitivity as indicated by the homeostasis model assessment of insulin resistance (HOMA-IR) (p < 0.05). LPL expression was up-regulated in the kidney, heart, quadriceps femoris, abdominal muscle and the visceral and subcutaneous adipose tissues but down-regulated in the liver - a condition in reverse to that seen in high-fat diet-induced obese rats without GA. With regard to lipid metabolism, GA administration led to significant hypotriglyceridemic and HDL-raising effects (p < 0.05), with a consistent reduction in serum free fatty acid, total cholesterol and LDL cholesterol and significant decrease in tissue lipid deposition across all studied tissue (p < 0.01).ConclusionIn conclusion, GA may be a potential compound in improving dyslipidaemia by selectively inducing LPL expression in non-hepatic tissues. Such up-regulation was accompanied by a GA-mediated improvement in insulin sensitivity, which may be associated with a decrease in tissue lipid deposition. The HDL-raising effect of GA suggests the antiatherosclerotic properties of GA.
Highlights
The metabolic syndrome, known as the insulin resistance syndrome, refers to the clustering of several risk factors for atherosclerotic cardiovascular disease
The heart showed the highest decrease with a fold difference of -4.184 ± 0.25, followed by the abdominal muscle (AM) (- 4.059 ± 0.31), kidney (-2.483 ± 0.32 fold), subcutaneous adipose tissue (SAT) (-2.924 ± 0.39 fold), quadriceps femoris (QF) (-1.970 ± 0.65) and visceral adipose tissue (VAT) (-1.361 ± 0.76)
The downregulation of lipoprotein lipase (LPL) in the adipose tissues, muscles and kidney under study may be due to inflammatory mediators such as tumour necrosis factor-alpha (TNF-a) which are found to be elevated in obesity and insulin resistant states [24]
Summary
The metabolic syndrome, known as the insulin resistance syndrome, refers to the clustering of several risk factors for atherosclerotic cardiovascular disease. The metabolic syndrome (MetS), known as the insulin resistance syndrome and syndrome X, refers to the clustering of several risk factors for atherosclerotic cardiovascular disease. Various studies have shown that with the development of IR, the production and activity of the enzyme lipoprotein lipase (LPL) is reduced [4,5]. Reduced LPL activity has been shown to lead to an inhibition in the lipolytic rate of the chylomicrons and the very-low-density lipoproteins (VLDL), triggering the development of hypertriglyceridaemia and the subsequent dyslipidaemia seen in the MetS [7,8].
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