ArticleDiabetologia2016
Genetic models rule out a major role of beta cell glycogen in the control of glucose homeostasis.
Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Impaired glucose tolerance and mild diabetes induce β-cell dysfunction in mice.Nature communications · 2026Article
- Contrasting Effects of Chronic Glucokinase Activation and Inhibition on Pancreatic Beta-Cell Function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Integrated in vitro, in silico, and in vivo approaches to elucidate the antidiabetic mechanisms of Cicer arietinum and Hordeum vulgare extract and secondary metabolites.Scientific reports · 2025Article
- Article
- Glycogen phosphorylase inhibition improves beta cell function.British journal of pharmacology · 2018Article
- Is Type 2 Diabetes a Glycogen Storage Disease of Pancreatic β Cells?Cell metabolism · 2017Review
- Identification of Differentially Expressed Micrornas Associate with Glucose Metabolism in Different Organs of Blunt Snout Bream (Megalobrama amblycephala).International journal of molecular sciences · 2017Article
- Protein targeting to glycogen is a master regulator of glycogen synthesis in astrocytes.IBRO reports · 2016Article
- Hyperglycaemia induces metabolic dysfunction and glycogen accumulation in pancreatic β-cells.Nature communications · 2016Article
- Role of glycogen metabolism in pancreatic islet beta cell function.Diabetologia · 2016Article
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7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisGlycogen accumulation occurs in beta cells of diabetic patients and has been proposed to partly mediate glucotoxicity-induced beta cell dysfunction. However, the role of glycogen metabolism in beta cell function and its contribution to diabetes pathophysiology remain poorly understood. We investigated the function of beta cell glycogen by studying glucose homeostasis in mice with (1) defective glycogen synthesis in the pancreas; and (2) excessive glycogen accumulation in beta cells.
methodsConditional deletion of the Gys1 gene and overexpression of protein targeting to glycogen (PTG) was accomplished by Cre-lox recombination using pancreas-specific Cre lines. Glucose homeostasis was assessed by determining fasting glycaemia, insulinaemia and glucose tolerance. Beta cell mass was determined by morphometry. Glycogen was detected histologically by periodic acid-Schiff's reagent staining. Isolated islets were used for the determination of glycogen and insulin content, insulin secretion, immunoblots and gene expression assays.
resultsGys1 knockout (Gys1 (KO)) mice did not exhibit differences in glucose tolerance or basal glycaemia and insulinaemia relative to controls. Insulin secretion and gene expression in isolated islets was also indistinguishable between Gys1 (KO) and controls. Conversely, despite effective glycogen overaccumulation in islets, mice with PTG overexpression (PTG(OE)) presented similar glucose tolerance to controls. However, under fasting conditions they exhibited lower glycaemia and higher insulinaemia. Importantly, neither young nor aged PTG(OE) mice showed differences in beta cell mass relative to age-matched controls. Finally, a high-fat diet did not reveal a beta cell-autonomous phenotype in either model. CONCLUSIONS/
interpretationGlycogen metabolism is not required for the maintenance of beta cell function. Glycogen accumulation in beta cells alone is not sufficient to trigger the dysfunction or loss of these cells, or progression to diabetes.
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