ArticleDiabetes2011
Drosophila insulin pathway mutants affect visual physiology and brain function besides growth, lipid, and carbohydrate metabolism.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 58 citations in OpenAlex.
- Preclinical research in obesity-associated metabolic diseases using in vitro, multicellular, and non-mammalian models.Journal of physiology and biochemistry · 2025Review
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- Upregulation of Tribbles decreases body weight and increases sleep duration.Disease models & mechanisms · 2023Article
- Vitamin B6 rescues insulin resistance and glucose-induced DNA damage caused by reduced activity of Drosophila PI3K.Journal of cellular physiology · 2022Article
- Exploring the link between Parkinson's disease and type 2 diabetes mellitus in Drosophila.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Review
- Metabolic Syndrome: Lessons from Rodent andBioMed research international · 2022Review
- The effects of high-monosaccharide diets on development and biochemical composition of white-eyed mutant strain of house cricket (Acheta domesticus).Scientific reports · 2021Article
- The Genetics of Diabetes: What We Can Learn fromInternational journal of molecular sciences · 2021Review
- Genetic manipulation of insulin/insulin-like growth factor signaling pathway activity has sex-biased effects on Drosophila body size.G3 (Bethesda, Md.) · 2021Article
- Article
- Subpopulation of Macrophage-Like Plasmatocytes Attenuates Systemic Growth via JAK/STAT in theFrontiers in immunology · 2020Article
- Insulin-Mediated Changes in Tau Hyperphosphorylation and Autophagy in aFrontiers in neuroscience · 2019Article
- Diet Composition Differentially Affects Insulin Pathway Compromised and Control Flies.BioMed research international · 2019Article
- Article
- Protective role of vitamin B6 (PLP) against DNA damage in Drosophila models of type 2 diabetes.Scientific reports · 2018Article
- Hobbit regulates intracellular trafficking to drive insulin-dependent growth duringDevelopment (Cambridge, England) · 2018Article
- Review
- REPTOR and REPTOR-BP Regulate Organismal Metabolism and Transcription Downstream of TORC1.Developmental cell · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveType 2 diabetes is the most common form of diabetes worldwide. Some of its complications, such as retinopathy and neuropathy, are long-term and protracted, with an unclear etiology. Given this problem, genetic model systems, such as in flies where type 2 diabetes can be modeled and studied, offer distinct advantages. RESEARCH DESIGN AND
methodsWe used individual flies in experiments: control and mutant individuals with partial loss-of-function insulin pathway genes. We measured wing size and tested body weight for growth phenotypes, the latter by means of a microbalance. We studied total lipid and carbohydrate content, lipids by a reaction in single fly homogenates with vanillin-phosphoric acid, and carbohydrates with an anthrone-sulfuric acid reaction. Cholinesterase activity was measured using the Ellman method in head homogenates from pooled fly heads, and electroretinograms with glass capillary microelectrodes to assess performance of central brain activity and retinal function.
resultsFlies with partial loss-of-function of insulin pathway genes have significantly reduced body weight, higher total lipid content, and sometimes elevated carbohydrate levels. Brain function is impaired, as is retinal function, but no clear correlation can be drawn from nervous system function and metabolic state.
conclusionsThese studies show that flies can be models of type 2 diabetes. They weigh less but have significant lipid gains (obese); some also have carbohydrate gains and compromised brain and retinal functions. This is significant because flies have an open circulatory system without microvasculature and can be studied without the complications of vascular defects.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.