High consumption of fructose rather than glucose promotes a diet-induced obese phenotype in Drosophila melanogaster

Comp Biochem Physiol A Mol Integr Physiol. 2015 Feb:180:75-85. doi: 10.1016/j.cbpa.2014.11.008. Epub 2014 Nov 15.

Abstract

During the last 20 years, there has been a considerable scientific debate about the possible mechanisms of induction of metabolic disorders by reducing monosaccharides such as glucose or fructose. In this study, we report the metabolic rearrangement in response to consumption of these monosaccharides at concentrations ranging from 0.25% to 20% in a Drosophila model. Flies raised on high-glucose diet displayed delay in pupation and increased developmental mortality compared with fructose consumers. Both monosaccharides at high concentrations promoted an obese-like phenotype indicated by increased fly body mass, levels of uric acid, and circulating and stored carbohydrates and lipids; and decreased percentage of water in the body. However, flies raised on fructose showed lower levels of circulating glucose and higher concentrations of stored carbohydrates, lipids, and uric acid. The preferential induction of obesity caused by fructose in Drosophila was associated with increased food consumption and reduced mRNA levels of DILP2 and DILP5 in the brain of adult flies. Our data show that glucose and fructose differently affect carbohydrate and lipid metabolism in Drosophila in part by modulation of insulin/insulin-like growth factor signaling. Some reported similarities with effects observed in mammals make Drosophila as a useful model to study carbohydrate influence on metabolism and development of metabolic disorders.

Keywords: Body composition; Fructose; Glucose; Insulin/IGF signaling; Obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diet
  • Drosophila Proteins / biosynthesis
  • Drosophila melanogaster / metabolism*
  • Fructose / administration & dosage
  • Fructose / metabolism*
  • Glucose / metabolism
  • Humans
  • Inhibitor of Apoptosis Proteins / biosynthesis
  • Lipid Metabolism / drug effects
  • Models, Animal
  • Obesity / chemically induced
  • Obesity / metabolism*
  • Obesity / pathology

Substances

  • DIAP2 protein, Drosophila
  • Drosophila Proteins
  • Inhibitor of Apoptosis Proteins
  • Fructose
  • Glucose