Dietary lipids and gene expression

2004 ◽  
Vol 32 (6) ◽  
pp. 999-1002 ◽  
Author(s):  
H.M. Roche
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Transcription Factors ◽  
Fatty Acid ◽  
Regulatory Element ◽  
Nuclear Factor Κb ◽  
Dietary Lipids ◽  
Dietary Fatty Acids ◽  
Dietary Fatty Acid ◽  
The Metabolic Syndrome

Nutrition is a key environmental factor that is particularly involved in the pathogenesis and progression of several polygenic, diet-related diseases. Nutrigenomics refers to the interaction between nutrition and the human genome. Dietary fatty acids interact with multiple nutrient-sensitive transcription factors. This explains the molecular basis of some of the health effects associated with altered dietary fatty acid composition. The metabolic syndrome is a very common condition, characterized by insulin resistance, abdominal obesity, dyslipidaemia and hypertension. It often precedes Type 2 diabetes mellitus, and is associated with a greater risk of cardiovascular disease. Several lines of evidence suggest that the interaction between nutrient-derived metabolic stressors and pro-inflammatory signals play an important role in the aetiology of insulin resistance and the development of the metabolic syndrome. This paper will address the interaction between several nutrient-sensitive transcription factors, including SREBP (sterol-regulatory-element-binding protein) and NFκB (nuclear factor κB), demonstrating how this interaction may be altered with dietary fatty acid interventions.

scholarly journals Calpain-10 interacts with plasma saturated fatty acid concentrations to influence insulin resistance in individuals with the metabolic syndrome

2011 ◽  
Vol 93 (5) ◽  
pp. 1136-1141 ◽  
Author(s):  
Pablo Perez-Martinez ◽  
Javier Delgado-Lista ◽  
Antonio Garcia-Rios ◽  
Jane F Ferguson ◽  
Hanne L Gulseth ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Saturated Fatty Acid ◽  
The Metabolic Syndrome ◽  
Calpain 10

Apoptosis in skeletal muscle myotubes is induced by ceramides and is positively related to insulin resistance

2006 ◽  
Vol 291 (6) ◽  
pp. E1341-E1350 ◽  
Author(s):  
Sarah M. Turpin ◽  
Graeme I. Lancaster ◽  
Ian Darby ◽  
Mark A. Febbraio ◽  
Matthew J. Watt
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Protein Content ◽  
The Metabolic Syndrome ◽  
Effector Caspase ◽  
Induced Apoptosis ◽  
Ceramide Accumulation

Fatty acid-induced apoptosis occurs in pancreatic β-cells and contributes to the metabolic syndrome. Skeletal muscle insulin resistance is mediated by fatty acid oversupply, which also contributes to the metabolic syndrome. Therefore, we examined whether fatty acids induce apoptosis in skeletal muscle myotubes, the proapoptotic signaling involved, and the effects on insulin sensitivity. Exposure of L6 myotubes to palmitate induced apoptosis, as demonstrated by increased caspase-3 activation, phosphatidylserine exposure on the plasma membrane, and terminal deoxynucleotide transferase dUTP nick end labeling and DNA laddering, both markers of DNA fragmentation. Ceramide content was concomitantly increased, indicating a potential role for ceramides in palmitate-induced apoptosis. Supporting this notion, reducing stearoyl-CoA desaturase-1 (SCD-1) protein content with short interfering RNA resulted in ceramide accumulation and was associated with increased apoptosis in the absence of palmitate. Furthermore, the membrane-permeable C2-ceramide enhanced apoptosis in myotubes, whereas the ceramide synthase inhibitor, fumonisin B1, abrogated the proapoptotic effects of palmitate. Insulin-stimulated glucose uptake was inhibited by palmitate treatment, whereas the addition of effector caspase inhibitors [Ac-DEVD-aldehyde (DEVD-CHO), Z-DQMD-FMK] independently restored >80% of the insulin-stimulated glucose uptake. These effects were observed independently from changes in the protein content of insulin signaling proteins, suggesting that proteosomal degradation is not involved in this process. We conclude that lipoapoptosis occurs in skeletal muscle myotubes, at least partially via de novo ceramide accumulation, and that inhibiting downstream apoptotic signaling improves glucose uptake in vitro.

scholarly journals Deepure Tea Improves High Fat Diet-Induced Insulin Resistance and Nonalcoholic Fatty Liver Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Jing-Na Deng ◽  
Juan Li ◽  
Hong-Na Mu ◽  
Yu-Ying Liu ◽  
Ming-Xia Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Hepatic Steatosis ◽  
Fatty Acid Synthesis ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Regulatory Element ◽  
Acid Synthesis ◽  
High Fat ◽  
The Metabolic Syndrome

This study was to explore the protective effects of Deepure tea against insulin resistance and hepatic steatosis and elucidate the potential underlying molecular mechanisms. C57BL/6 mice were fed with a high fat diet (HFD) for 8 weeks to induce the metabolic syndrome. In the Deepure tea group, HFD mice were administrated with Deepure tea at 160 mg/kg/day by gavage for 14 days. The mice in HFD group received water in the same way over the same period. The age-matched C57BL/6 mice fed with standard chow were used as normal control. Compared to the mice in HFD group, mice that received Deepure tea showed significantly reduced plasma insulin and improved insulin sensitivity. Deepure tea increased the expression of insulin receptor substrate 2 (IRS-2), which plays an important role in hepatic insulin signaling pathway. Deepure tea also led to a decrease in hepatic fatty acid synthesis and lipid accumulation, which were mediated by the downregulation of sterol regulatory element binding protein 1c (SREBP-1c), fatty acid synthesis (FAS), and acetyl-CoA carboxylase (ACC) proteins that are involved in liver lipogenesis. These results suggest that Deepure tea may be effective for protecting against insulin resistance and hepatic steatosis via modulating IRS-2 and downstream signaling SREBP-1c, FAS, and ACC.

scholarly journals Mechanisms of the components of the metabolic syndrome that predispose to diabetes and atherosclerotic CVD

2007 ◽  
Vol 66 (1) ◽  
pp. 82-95 ◽  
Author(s):  
Robert H. Eckel
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Inflammatory Cytokines ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
The Metabolic Syndrome ◽  
Pro Inflammatory Cytokines

The metabolic syndrome represents a summation of obesity-driven risk factors for atherosclerotic CVD and type 2 diabetes. Definitions of the syndrome vary but in general agree closely in identifying subjects. The relationships between the metabolic syndrome and atherosclerotic CVD and diabetes also vary, with relative risks of approximately 1·5–3·0 and approximately 3·0–5·0 respectively. Insulin resistance appears to explain much of the pathophysiology of the syndrome. Both increased fatty acid flux and an excess of circulating pro-inflammatory cytokines are likely mediators. With increased waist circumference, increases in fatty acid delivery to the liver result in higher rates of hepatic glucose production and increases in the secretion of apoB-containing lipoproteins. Concomitant changes in HDL ensue, including a replacement of the cholesterol content with TAG, an accelerated clearance from the plasma and thus a reduced number of HDL particles. Typically also present are increases in small dense LDL. Hypertension in part relates to the insulin resistance, but may involve other mechanisms. Impaired fasting glucose often relates to defects in insulin secretion in addition to insulin resistance, and probably more than any other component of the syndrome predicts the increased incidence of type 2 diabetes. Although not included in the diagnostic criteria, increases in pro-inflammatory cytokines and pro-thrombotic factors, in addition to decreases in plasma adiponectin, may also contribute to the increased incidence of atherosclerotic CVD and diabetes. In general, the greater the number of metabolic syndrome components, the greater the risk for these outcomes. The cytokines and pro-thrombotic factors also appear to contribute.

scholarly journals Adipocyte Fatty Acid–Binding Protein Is a Plasma Biomarker Closely Associated with Obesity and Metabolic Syndrome

2006 ◽  
Vol 52 (3) ◽  
pp. 405-413 ◽  
Author(s):  
Aimin Xu ◽  
Yu Wang ◽  
Jian Yu Xu ◽  
David Stejskal ◽  
Sidney Tam ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Human Serum ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Model Assessment ◽  
Fatty Acid Binding ◽  
Acid Binding Protein ◽  
The Metabolic Syndrome

Abstract Background: Adipocyte fatty acid–binding protein (A-FABP) is traditionally thought to be a cytosolic fatty acid chaperone expressed in adipocytes. Mice with targeted disruption of the A-FABP gene exhibit a striking phenotype with strong protection from insulin resistance, hyperglycemia, and atherosclerosis. The clinical relevance of these findings remains to be confirmed. Methods: We used tandem mass spectrometry–based proteomic analysis to identify proteins secreted from adipocytes and present in human serum. We measured serum A-FABP concentrations in 229 persons (121 men and 108 women; age range, 33–72 years), including 100 lean [body mass index (BMI) <25 kg/m2] and 129 overweight/obese individuals (BMI >25 kg/m2) selected from a previous cross-sectional study. Results: A-FABP was released from adipocytes and was abundantly present in human serum. Mean (SD) circulating concentrations of A-FABP were significantly higher in overweight/obese than in lean persons [32.3 (14.8) vs 20.0 (9.8) μg/L; P <0.001]. Age- and sex-adjusted serum A-FABP concentrations correlated positively (P <0.005) with waist circumference, blood pressure, dyslipidemia, fasting insulin, and the homeostasis model assessment insulin resistance index. Moreover, we observed a significant increase in A-FABP concentrations corresponding with increases in the number of components of the metabolic syndrome (P <0.05). Conclusions: A-FABP is a circulating biomarker closely associated with obesity and components of the metabolic syndrome, and measurement of serum concentrations of A-FABP might be useful for clinical diagnosis of obesity-related metabolic and cardiovascular disorders.

scholarly journals Fatty acid transport receptor soluble CD36 and dietary fatty acid pattern in type 2 diabetic patients: a comparative study

2018 ◽  
Vol 119 (2) ◽  
pp. 153-162 ◽  
Author(s):  
Merve Ekici ◽  
Ucler Kisa ◽  
Senay Arikan Durmaz ◽  
Elif Ugur ◽  
Reyhan Nergiz-Unal
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Fatty Acid Pattern ◽  
Food Preferences ◽  
Dietary Fatty Acids ◽  
Dietary Fatty Acid ◽  
Diabetic Patients ◽  
Fatty Acid Transport ◽  
Type 2 Dm

AbstractRecently, it has been remarked that dietary fatty acids and fatty acid receptors might be involved in the aetiology of diabetes. Therefore, this study was conducted to determine the relationship between dietary fatty acid pattern, fatty food preferences and soluble CD36 (sCD36) and insulin resistance in type 2 diabetes mellitus (DM). The study was carried out with thirty-eight newly diagnosed type 2 DM patients and thirty-seven healthy volunteers, aged 30–65 years. In the study, socio-demographic characteristics, dietary fat type and fatty acid pattern of individuals were recorded. After anthropometric measurements were taken, blood CD36, glucose, TAG and insulin levels were analysed. The results showed that although the type of fatty acid intake did not differ between the groups (P>0·05), the consumption of olive oil in the type 2 DM group was lower than the control group (P<0·05). Mean blood glucose, insulin, insulin resistance, TAG and sCD36 levels were determined to be higher in the type 2 DM group (P<0·05). However, there was no correlation between sCD36 levels and homeostatic model assessment of insulin resistance (HOMA-IR) value, blood insulin and TAG levels, waist circumference, dietary fatty acid pattern and food preferences in the type 2 DM group (P>0·05). Crucially, elevated sCD36 levels increased the type 2 DM risk (OR 1·21, P<0·05). In conclusion, sCD36 level may be a possible biomarker, independent from the dietary fatty acid pattern, for type 2 DM owing to its higher levels in these patients. Therefore, the new insights make CD36 attractive as a therapeutic target for diabetes.

scholarly journals Glucocorticoids and fatty acid metabolism in humans: fuelling fat redistribution in the metabolic syndrome

2008 ◽  
Vol 197 (2) ◽  
pp. 189-204 ◽  
Author(s):  
David P Macfarlane ◽  
Shareen Forbes ◽  
Brian R Walker
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Glucose Metabolism ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Hepatic Insulin Resistance ◽  
Induce Insulin Resistance ◽  
The Metabolic Syndrome

Glucocorticoid hormones constitute an integral component of the response to stress, and many of the manifestations of glucocorticoid excess (Cushing's syndrome) are predictable on the basis of their acute effects to raise blood pressure, induce insulin resistance, increase protein catabolism and elevate plasma glucose. However, it appears to be a paradox that the acute lipolytic effect of glucocorticoids is not manifest in long-term weight loss in humans. The effects of glucocorticoids on glucose metabolism are well characterised, involving impaired peripheral glucose uptake and hepatic insulin resistance, and there is mounting evidence that subtle abnormalities in glucocorticoid concentrations in the plasma and/or in tissue sensitivity to glucocorticoids are important in metabolic syndrome. The effects of glucocorticoids on fatty acid metabolism are less well understood than their influence on glucose metabolism. In this article, we review the literature describing the effects of glucocorticoids on fatty acid metabolism, with particular reference to in vivo human studies. We consider the implications for contrasting acute versus chronic effects of glucocorticoids on fat accumulation, effects in different adipose depots and the potential role of glucocorticoid signalling in the pathogenesis and therapy of metabolic syndrome.

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