Abdominal Obesity in Older Women: Potential Role for Disrupted Fatty Acid Reesterification in Insulin Resistance

AbstractThe metabolic impact of circulating fatty acids (FAs) in patients requiring hemodialysis (HD) is unknown. We investigated the associations between plasma triglyceride (TG) FAs and markers of inflammation, insulin resistance, nutritional status and body composition. Plasma TG-FAs were measured using gas chromatography in 341 patients on HD (age = 55.2 ± 14.0 years and 54.3% males). Cross-sectional associations of TG-FAs with 13 markers were examined using multivariate linear regression adjusted for potential confounders. Higher levels of TG saturated fatty acids were associated with greater body mass index (BMI, r = 0.230), waist circumference (r = 0.203), triceps skinfold (r = 0.197), fat tissue index (r = 0.150), serum insulin (r = 0.280), and homeostatic model assessment of insulin resistance (r = 0.276), but lower malnutrition inflammation score (MIS, r = − 0.160). Greater TG monounsaturated fatty acid levels were associated with lower lean tissue index (r = − 0.197) and serum albumin (r = − 0.188), but higher MIS (r = 0.176). Higher levels of TG n-3 polyunsaturated fatty acids (PUFAs) were associated with lower MIS (r = − 0.168) and interleukin-6 concentrations (r = − 0.115). Higher levels of TG n-6 PUFAs were associated with lower BMI (r = − 0.149) but greater serum albumin (r = 0.112). In conclusion, TG monounsaturated fatty acids were associated with poor nutritional status, while TG n-3 PUFAs were associated with good nutritional status. On the other hand, TG saturated fatty acids and TG n-6 PUFAs had both favorable and unfavorable associations with nutritional parameters.

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POTENTIAL ROLE OF REDOX SENSITIVE SERINE KINASE PATHWAYS IN THE PATHOGENESIS OF INSULIN RESISTANCE IN RHEUMATOID ARTHRITIS

International Journal of Biomedical and Advance Research ◽

10.7439/ijbar.v2i8.40 ◽

2011 ◽

Vol 2 (8) ◽

Author(s):

R. Vinayagamoorthi ◽

Zachariah Bobby ◽

A. Thiruvaimozhi

Keyword(s):

Rheumatoid Arthritis ◽

Insulin Resistance ◽

Potential Role ◽

Serine Kinase

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Interaction of physical activity and diet: implications for insulin-glucose dynamics

Public Health Nutrition ◽

10.1017/s136898009900049x ◽

1999 ◽

Vol 2 (3a) ◽

pp. 363-368 ◽

Cited By ~ 18

Author(s):

Jean-Jacques Grimm

Keyword(s):

Insulin Resistance ◽

Cardiovascular Risk ◽

Fatty Acid ◽

Glycogen Synthase ◽

Insulin Resistance Syndrome ◽

Low Fat ◽

Exercise Interventions ◽

High Carbohydrate ◽

Fat Diets

AbstractIn Western countries 25–35% of the population have insulin resistance syndrome characteristics.The defects most likely to explain the insulin resistance of the insulin resistance syndrome include: 1) the glucose transport system of skeletal muscle (GLUT-4) and its different signalling proteins and enzymes; 2) glucose phosphorylation by hexokinase; 3) glycogen synthase activity and 4) competition between glucose and fatty acid oxidation (glucose-fatty acid cycle).High carbohydrate/low fat diets deteriorate insulin sensitivity on the short term. Howewer, on the long term, high fat/low carbohydrate diets have a lower satiating power, induce low leptin levels and eventually lead to higher energy consumption, obesity and more insulin resistance. Moderately high-carbohydrate (45–55% of the daily calories)/low-fat diets seem to be a good choice with regard to the prevention of diabetes and cardiovascular risk factors as far as the carbohydrates are rich in fibers.Long-term interventions with regular exercise programs show a 1/3 decrease in the appearance of overt diabetes in glucose intolerant subjects. Furthermore, diet and exercise interventions "normalise" the mortality rate of patients with impared glucose tolerance.Therefore, moderately high carbohydrate/low fat diets are most likely to prevent obesity and type 2 diabetes. Triglycerides should be monitored and, in some cases, a part of the carbohydrates could be replaced by fat rich in monounsaturated fatty acids. However, total caloric intake is of utmost importance, as weight gain is the major determinant for the onset of insulin resistance and glucose intolerance.Regular (when possible daily) exercise, decreases cardiovascular risk. With regard to insulin resistance, resistance training seems to offer some advantages over aerobic endurance activities.

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Effect of Abdominal Obesity on Insulin Resistance and the Components of the Metabolic Syndrome: Evidence Supporting Obesity as the Central Feature

Obesity Surgery ◽

10.1381/096089203322509255 ◽

2003 ◽

Vol 13 (5) ◽

pp. 699-705 ◽

Cited By ~ 26

Author(s):

Çavlan Türkoglu ◽

Belgin Süsleyici Duman ◽

Demet Günay ◽

Penbe Çagatay ◽

Remzi Özcan ◽

...

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

Abdominal Obesity ◽

Central Feature ◽

The Metabolic Syndrome

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Abdominal obesity, insulin resistance, and cardiovascular risk in pre-diabetes and type 2 diabetes

European Heart Journal Supplements ◽

10.1093/eurheartj/sul004 ◽

2006 ◽

Vol 8 (suppl_B) ◽

pp. B20-B25 ◽

Cited By ~ 21

Author(s):

Steven M. Haffner

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Cardiovascular Risk ◽

Abdominal Obesity

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Insulin-independent regulation of hepatic triglyceride synthesis by fatty acids

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1423952112 ◽

2015 ◽

Vol 112 (4) ◽

pp. 1143-1148 ◽

Cited By ~ 118

Author(s):

Daniel F. Vatner ◽

Sachin K. Majumdar ◽

Naoki Kumashiro ◽

Max C. Petersen ◽

Yasmeen Rahimi ◽

...

Keyword(s):

Insulin Resistance ◽

Fatty Acids ◽

Fatty Acid ◽

Insulin Signaling ◽

Plasma Fatty Acid ◽

Hepatic Triglyceride ◽

Triglyceride Synthesis ◽

Hepatic Glucose ◽

Acid Esterification ◽

Fatty Acid Esterification

A central paradox in type 2 diabetes is the apparent selective nature of hepatic insulin resistance—wherein insulin fails to suppress hepatic glucose production yet continues to stimulate lipogenesis, resulting in hyperglycemia, hyperlipidemia, and hepatic steatosis. Although efforts to explain this have focused on finding a branch point in insulin signaling where hepatic glucose and lipid metabolism diverge, we hypothesized that hepatic triglyceride synthesis could be driven by substrate, independent of changes in hepatic insulin signaling. We tested this hypothesis in rats by infusing [U-13C] palmitate to measure rates of fatty acid esterification into hepatic triglyceride while varying plasma fatty acid and insulin concentrations independently. These experiments were performed in normal rats, high fat-fed insulin-resistant rats, and insulin receptor 2′-O-methoxyethyl chimeric antisense oligonucleotide-treated rats. Rates of fatty acid esterification into hepatic triglyceride were found to be dependent on plasma fatty acid infusion rates, independent of changes in plasma insulin concentrations and independent of hepatocellular insulin signaling. Taken together, these results obviate a paradox of selective insulin resistance, because the major source of hepatic lipid synthesis, esterification of preformed fatty acids, is primarily dependent on substrate delivery and largely independent of hepatic insulin action.

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