Effects of dietary fatty acids on insulin sensitivity and secretion

Abstract

Globalization and global market have contributed to increased consumption of high-fat, energy-dense diets, particularly rich in saturated fatty acids( SFAs). Polyunsaturated fatty acids (PUFAs) regulate fuel partitioning within the cells by inducing their own oxidation through the reduction of lipogenic gene expression and the enhancement of the expression of those genes controlling lipid oxidation and thermogenesis. Moreover, PUFAs prevent insulin resistance by increasing membrane fluidity and GLUT4 transport. In contrast, SFAs are stored in non-adipocyte cells as triglycerides (TG) leading to cellular damage as a sequence of their lipotoxicity. Triglyceride accumulation in skeletal muscle cells (IMTG) derives from increased FA uptake coupled with deficient FA oxidation. High levels of circulating FAs enhance the expression of FA translocase the FA transport proteins within the myocites. The biochemical mechanisms responsible for lower fatty acid oxidation involve reduced carnitine palmitoyl transferase (CPT) activity, as a likely consequence of increased intracellular concentrations of malonyl-CoA; reduced glycogen synthase activity; and impairment of insulin signalling and glucose transport. The depletion of IMTG depots is strictly associated with an improvement of insulin sensitivity, via a reduced acetyl-CoA carboxylase (ACC) mRNA expression and an increased GLUT4 expression and pyruvate dehydrogenase (PDH) activity. In pancreatic islets, TG accumulation causes impairment of insulin secretion. In rat models, beta-cell dysfunction is related to increased triacylglycerol content in islets, increased production of nitric oxide, ceramide synthesis and beta-cell apoptosis. The decreased insulin gene promoter activity and binding of the pancreas-duodenum homeobox-1 (PDX-1) transcription factor to the insulin gene seem to mediate TG effect in islets. In humans, acute and prolonged effects of FAs on glucose-stimulated insulin secretion have been widely investigated as well as the effect of high-fat diets on insulin sensitivity and secretion and on the development of type 2 diabetes.

Evaluation of antidiabetic properties of cactus pear seed oil in rats

“…The omega-3 fatty acids increase the insulin secretion stimulated by D-glucose by contact with Langerhans islet beta cells (Oguzhan et al, 2006). In addition, polyunsaturated fatty acids enhance cell membrane fluidity and GLUT4 transporter expression (Manco et al, 2004). Moreover, polyunsaturated fatty acids improve insulin-induced glucose uptake on insulin-sensitive cells (3T3-L1 adipocytes) by increasing GLUT1 and GLUT4 plasma membrane density (Nugent et al, 2001).…”

Polyunsaturated fatty acids: From diet to binding to ppars and other nuclear receptors

“…The nuclear actions of PUFAs is established in liver cells (Jump et al, 2005), in pancreas (Manco et al, 2004), immune system (Calder, 2003), brain (Uauy and Calderon, 2003), adipose tissue (Al-Hasani and Joost, 2005) and heart (Vanden Heuvel, 2004), and the possibility of counteracting human diseases by dietary FAs, particularly n-3 PUFAs, has been largely investigated, although their therapeutic effects are still unclear (De Caterina et al, 2006;Engler and Engler, 2006;Hooper et al, 2006;Lombardo and Chicco, 2006;Grynberg, 2005;Mills et al, 2005;Rodriguez-Cruz et al, 2005;Sekiya et al, 2003). It is important to remember that the effects of PUFAs are due to changes in membrane FA composition and subsequent alterations in hormonal signalling, as well as to their direct, membrane independent influence on molecular events that govern gene expression.…”

Investigation of the effects of peppermint (Mentha piperita) on the biochemical and anthropometric profile of university students

“…development of dyslipidemias, diabetes, arterial hypertension, obesity, metabolic syndrome (MS) and vascular diseases (MANCO et al, 2004;MERCHANT et al, 2007;HOENIG, 2008;HSIEH et al, 2008;FRICK et al, 2008).…”