title: Effects of dietary glycaemic index on adiposity, glucose homoeostasis, and plasma lipids in animals.
abstract: BACKGROUND
  Clinical studies suggest a role for dietary glycaemic index (GI) in bodyweight regulation and diabetes risk. However, partly because manipulation of GI can produce changes in potentially confounding dietary factors such as fibre content, palatability, and energy density, its relevance to human health remains controversial. This study examined the independent effects of GI in animals.
  
  
  METHODS
  Partially pancreatectomised male Sprague-Dawley rats were given diets with identical nutrients, except for the type of starch: high-GI (n=11) or low-GI (n=10). The animals were fed in a controlled way to maintain the same mean bodyweight in the two groups for 18 weeks. Further experiments examined the effects of GI in rats in a cross-over design and C57BL/6J mice in a parallel design.
  
  
  RESULTS
  Despite having similar mean bodyweight (547.9 [SE 13.4] vs 549.2 [15.2] g), rats given high-GI food had more body fat (97.8 [13.6] vs 57.3 [7.2] g; p=0.0152) and less lean body mass (450.1 [9.6] vs 491.9 [11.7] g; p=0.0120) than those given low-GI food. The high-GI group also had greater increases over time in the areas under the curve for blood glucose and plasma insulin after oral glucose, lower plasma adiponectin concentrations, higher plasma triglyceride concentrations, and severe disruption of islet-cell architecture. Mice on the high-GI diet had almost twice the body fat of those on the low-GI diet after 9 weeks.
  
  
  CONCLUSIONS
  These findings provide a mechanistic basis for interpretation of studies of GI in human beings.
  
  
  CONCLUSIONS
  The term GI describes how a food, meal, or diet affects blood sugar during the postprandial period. GI as an independent factor can cause obesity and increase risks of diabetes and heart disease in animals. Use of low-GI diets in prevention and treatment of human disease merits thorough examination.
authors.affiliation: Department of Medicine, Children's Hospital, Boston, MA, USA. david.ludwig@childrens.harvard.edu
authors.forename: Dorota B
authors.initials: DB
authors.lastname: Pawlak
authors.forename: Jake A
authors.initials: JA
authors.lastname: Kushner
authors.forename: David S
authors.initials: DS
authors.lastname: Ludwig
mesh_terms: D052242:Adiponectin; D000273:Adipose Tissue / Q000033:anatomy & histology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001823:Body Composition; D001835:Body Weight; D004040:Dietary Carbohydrates / Q000009:adverse effects*; D005951:Glucose Tolerance Test; D038321:Glycemic Index; D006706:Homeostasis; D007328:Insulin / Q000097:blood; D036341:Intercellular Signaling Peptides and Proteins; D007515:Islets of Langerhans / Q000473:pathology; D020738:Leptin / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000209:etiology / Q000378:metabolism*; D010180:Pancreatectomy; D019518:Postprandial Period; D011506:Proteins / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood*
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D004040:Dietary Carbohydrates; D007328:Insulin; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin; D011506:Proteins; D014280:Triglycerides