A high-sugar diet produces obesity and insulin resistance in wild-type Drosophila

Insulin-resistant, 'type 2' diabetes (T2D) results from a complex interplay between genes and environment. In particular, both caloric excess and obesity are strongly associated with T2D across many genetic backgrounds. To gain insights into how dietary excess affects insulin resistance, w...

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Bibliographic Details
Published in:Disease models & mechanisms 2011-11, Vol.4 (6), p.842-849
Main Authors: Musselman, Laura Palanker, Fink, Jill L, Narzinski, Kirk, Ramachandran, Prasanna Venkatesh, Hathiramani, Sumitha Sukumar, Cagan, Ross L, Baranski, Thomas J
Format: Article
Language:English
Subjects:
Ablation
Adults
Animals
Calories
Carbohydrate Metabolism - drug effects
Carbohydrate Metabolism - genetics
Diabetes
Diet
Dietary Carbohydrates - pharmacology
Drosophila melanogaster - drug effects
Drosophila melanogaster - genetics
Feeding Behavior - drug effects
Food
Gene Expression Regulation - drug effects
Genomes
Glucose
Hyperglycemia
Hyperglycemia - complications
Hyperglycemia - genetics
Hyperglycemia - pathology
Insects
Insulin resistance
Insulin Resistance - genetics
Lipid Metabolism - drug effects
Lipid Metabolism - genetics
Metabolism
Obesity
Obesity - complications
Obesity - genetics
Obesity - pathology
Physiology
Proteins
Research Report
Sucrose
Transcription, Genetic - drug effects
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Summary:Insulin-resistant, 'type 2' diabetes (T2D) results from a complex interplay between genes and environment. In particular, both caloric excess and obesity are strongly associated with T2D across many genetic backgrounds. To gain insights into how dietary excess affects insulin resistance, we studied the simple model organism Drosophila melanogaster. Larvae reared on a high-sugar diet were hyperglycemic, insulin resistant and accumulated fat--hallmarks of T2D--compared with those reared on control diets. Excess dietary sugars, but not fats or proteins, elicited insulin-resistant phenotypes. Expression of genes involved in lipogenesis, gluconeogenesis and β-oxidation was upregulated in high-sugar-fed larvae, as were FOXO targets, consistent with known mechanisms of insulin resistance in humans. These data establish a novel Drosophila model of diet-induced insulin resistance that bears strong similarity to the pathophysiology of T2D in humans.
ISSN:1754-8403
1754-8411
DOI:10.1242/dmm.007948