Carbohydrate-induced manipulation of insulin sensitivity independently of intramyocellular lipids

• Published in: British journal of nutrition 2003-03, Vol.89 (3), p.365-374
• Main Authors: Goff, Louise M., Frost, Gary S., Hamilton, Gavin, Thomas, E. Louise, Dhillo, Waljit S., Dornhorst, Anne, Bell, Jimmy D.
• Format: Article
• Language: English
• Subjects: Adult; Anthropometry; Biological and medical sciences; Blood Glucose - metabolism; Carbohydrate; Carbohydrates; Diabetes; Dietary Carbohydrates - administration & dosage; Fasting - blood; Fatty acids; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; Glucose; Glucose Tolerance Test; Glycaemic index; Glycemic Index; Health care; Humans; Insulin resistance; Insulin Resistance - physiology; Insulin sensitivity; Intervention; Intramyocellular lipids; Lipid Metabolism; Lipids; Magnetic Resonance Spectroscopy; Male; Metabolism; Middle Aged; Muscle, Skeletal - metabolism; Nutrition research; Prospective Studies; Spectrum analysis; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 0007-1145; 1475-2662
• DOI: 10.1079/BJN2002789

Subjects with insulin resistance have been shown to have higher storage levels of intramyocellular lipid (IMCL) than their insulin-sensitive counterparts. It has been proposed that elevated IMCL stores may be the main cause of insulin resistance. The aim of the present study was to ascertain whether there is a causal relationship between IMCL storage and insulin resistance. IMCL storage was assessed using magnetic resonance spectroscopy and insulin sensitivity was assessed by performing an oral glucose tolerance test. A 4-week intervention of reduction of dietary glycaemic index was used to manipulate insulin sensitivity in a cohort of healthy volunteers; the effects of this intervention on IMCL were measured after 4 weeks of intervention. Significant improvements in the insulin sensitivity index occurred following the dietary intervention (baseline 7·8 (sem 1·11) v. post-intervention 9·7 (sem 1·11), P=0·02). However, there were no changes in IMCL storage levels, suggesting that insulin sensitivity can be manipulated independently of IMCL. This suggests that in healthy volunteers, insulin sensitivity is independent of IMCL storage and the high storage levels that have been found in insulin-resistant subjects may occur as a consequence rather than a cause of insulin resistance.