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Energy restriction prevents the development of type 2 diabetes in Zucker diabetic fatty rats: coordinated patterns of gene expression for energy metabolism in insulin-sensitive tissues and pancreatic islets determined by oligonucleotide microarray analysis.

Abstract

Energy restriction (ER) causes metabolic improvement in the prediabetic and diabetic state. Little information exists on the mechanism of action of ER, for example, on the changes at the transcriptional gene level in insulin-sensitive tissues. To gain further insight, we have investigated changes in gene expressions in skeletal muscle, liver, fat, and pancreatic islets after ER in male Zucker diabetic fatty rats. Eighteen Zucker diabetic fatty rats were divided at the age of 7 weeks into a control group (ad libitum diet) and an ER group (30% ER compared with the control group). Blood glucose, weight, and food intake were measured weekly. After 5 weeks, blood samples, and skeletal muscle, liver, visceral fat (epididymal fat pads), and islets tissue were collected. Gene expression was quantified with high-density oligonucleotide, microarray GeneChip technology. ER ameliorated the development of hyperglycemia, increased the levels of plasma insulin, and reduced plasma total cholesterol and the glucagon-insulin ratio (P < .05). In skeletal muscle, the expression of 55 genes increased and 245 decreased involving genes related to glucose metabolism (eg, phosphorylase kinase, pyruvate dehydrogenase kinase 4), lipid metabolism (eg, carnitine palmitoyltransferase 1, fatty acid transporter), and signaling pathways (eg, mitogen-activated protein kinases, protein kinase C). In the liver, the expression of 123 genes increased and 103 decreased involving genes related primarily to lipid metabolism. In pancreatic islets, the expression of 110 genes increased and that of 127 decreased, whereas in visceral fat, the expression of 279 genes increased and that of 528 decreased. ER counteracts the development of diabetes and causes changes in the expression of multiple genes involved in glucose and lipid metabolism in skeletal muscle, liver, and pancreatic islets, which may play an important role for the prevention of diabetes.

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  • Authors+Show Affiliations

    ,

    Department of Endocrinology and Metabolism C, Aarhus Sygehus THG, Tage Hansens Gade 2, 8000 Aarhus C, Denmark. michele.colombo@ki.au.dk

    , , , , ,

    Source

    MeSH

    Adipose Tissue
    Animals
    Blood Glucose
    Body Weight
    Caloric Restriction
    Cell Nucleus
    Diabetes Mellitus, Type 2
    Energy Metabolism
    Hypoglycemic Agents
    In Vitro Techniques
    Insulin
    Islets of Langerhans
    Liver
    Male
    Muscle, Skeletal
    Oligonucleotide Array Sequence Analysis
    RNA, Messenger
    Rats
    Rats, Zucker

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    16324918

    Citation

    Colombo, Michele, et al. "Energy Restriction Prevents the Development of Type 2 Diabetes in Zucker Diabetic Fatty Rats: Coordinated Patterns of Gene Expression for Energy Metabolism in Insulin-sensitive Tissues and Pancreatic Islets Determined By Oligonucleotide Microarray Analysis." Metabolism: Clinical and Experimental, vol. 55, no. 1, 2006, pp. 43-52.
    Colombo M, Kruhoeffer M, Gregersen S, et al. Energy restriction prevents the development of type 2 diabetes in Zucker diabetic fatty rats: coordinated patterns of gene expression for energy metabolism in insulin-sensitive tissues and pancreatic islets determined by oligonucleotide microarray analysis. Metab Clin Exp. 2006;55(1):43-52.
    Colombo, M., Kruhoeffer, M., Gregersen, S., Agger, A., Jeppesen, P., Oerntoft, T., & Hermansen, K. (2006). Energy restriction prevents the development of type 2 diabetes in Zucker diabetic fatty rats: coordinated patterns of gene expression for energy metabolism in insulin-sensitive tissues and pancreatic islets determined by oligonucleotide microarray analysis. Metabolism: Clinical and Experimental, 55(1), pp. 43-52.
    Colombo M, et al. Energy Restriction Prevents the Development of Type 2 Diabetes in Zucker Diabetic Fatty Rats: Coordinated Patterns of Gene Expression for Energy Metabolism in Insulin-sensitive Tissues and Pancreatic Islets Determined By Oligonucleotide Microarray Analysis. Metab Clin Exp. 2006;55(1):43-52. PubMed PMID: 16324918.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Energy restriction prevents the development of type 2 diabetes in Zucker diabetic fatty rats: coordinated patterns of gene expression for energy metabolism in insulin-sensitive tissues and pancreatic islets determined by oligonucleotide microarray analysis. AU - Colombo,Michele, AU - Kruhoeffer,Mogens, AU - Gregersen,Soeren, AU - Agger,Andreas, AU - Jeppesen,PerBendix, AU - Oerntoft,Torben, AU - Hermansen,Kjeld, PY - 2004/04/20/received PY - 2005/07/24/accepted PY - 2005/12/6/pubmed PY - 2006/2/16/medline PY - 2005/12/6/entrez SP - 43 EP - 52 JF - Metabolism: clinical and experimental JO - Metab. Clin. Exp. VL - 55 IS - 1 N2 - Energy restriction (ER) causes metabolic improvement in the prediabetic and diabetic state. Little information exists on the mechanism of action of ER, for example, on the changes at the transcriptional gene level in insulin-sensitive tissues. To gain further insight, we have investigated changes in gene expressions in skeletal muscle, liver, fat, and pancreatic islets after ER in male Zucker diabetic fatty rats. Eighteen Zucker diabetic fatty rats were divided at the age of 7 weeks into a control group (ad libitum diet) and an ER group (30% ER compared with the control group). Blood glucose, weight, and food intake were measured weekly. After 5 weeks, blood samples, and skeletal muscle, liver, visceral fat (epididymal fat pads), and islets tissue were collected. Gene expression was quantified with high-density oligonucleotide, microarray GeneChip technology. ER ameliorated the development of hyperglycemia, increased the levels of plasma insulin, and reduced plasma total cholesterol and the glucagon-insulin ratio (P < .05). In skeletal muscle, the expression of 55 genes increased and 245 decreased involving genes related to glucose metabolism (eg, phosphorylase kinase, pyruvate dehydrogenase kinase 4), lipid metabolism (eg, carnitine palmitoyltransferase 1, fatty acid transporter), and signaling pathways (eg, mitogen-activated protein kinases, protein kinase C). In the liver, the expression of 123 genes increased and 103 decreased involving genes related primarily to lipid metabolism. In pancreatic islets, the expression of 110 genes increased and that of 127 decreased, whereas in visceral fat, the expression of 279 genes increased and that of 528 decreased. ER counteracts the development of diabetes and causes changes in the expression of multiple genes involved in glucose and lipid metabolism in skeletal muscle, liver, and pancreatic islets, which may play an important role for the prevention of diabetes. SN - 0026-0495 UR - https://www.unboundmedicine.com/medline/citation/16324918/Energy_restriction_prevents_the_development_of_type_2_diabetes_in_Zucker_diabetic_fatty_rats:_coordinated_patterns_of_gene_expression_for_energy_metabolism_in_insulin_sensitive_tissues_and_pancreatic_islets_determined_by_oligonucleotide_microarray_analysis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0026-0495(05)00293-3 DB - PRIME DP - Unbound Medicine ER -