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The Gut: A Key to the Pathogenesis of Type 2 Diabetes?

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  1. Metabolic Health in Severely Obese Subjects: A Descriptive Study

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Determinants of Fasting Hyperglucagonemia in Patients with Type 2 Diabetes and Nondiabetic Control Subjects

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  3. In Vivo and Ex Vivo Inflammatory Markers of Common Metabolic Phenotypes in Humans

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  4. Relationship Between Two Common Lipoprotein Lipase Variants and the Metabolic Syndrome and Its Individual Components

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  5. Determinants of obesity among men with the lewis double-negative blood group: a genetic marker of obesity-the Copenhagen Male Study

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  1. The Effects of Dual GLP-1/GIP Receptor Agonism on Glucagon Secretion-A Review

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  2. Glucagon Receptor Signaling and Glucagon Resistance

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  3. Continuous glucose monitoring in pregnant women with type 1 diabetes: an observational cohort study of 186 pregnancies

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In this communication we discuss the role of the gut for the development of type 2 diabetes mellitus (T2DM). Gastric emptying rates importantly determine postprandial glucose excursions and regulate postprandial secretion of the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide-1 (GLP-1). It thereby also determines their powerful, amplifying effect on glucose-induced insulin secretion and thus the ability of the body to regulate glucose disposal. Although disturbances in gastric emptying are not consistent findings in type 2 diabetes, the incretin system is seriously impaired, probably associated with insulin resistance and obesity. Both of the incretin hormones lose (part of) their insulinotropic activity resulting, together with (genetically) defective beta cell function, in the impaired postprandial insulin secretion of T2DM. In addition, glucagon responses are inappropriately increased and importantly contribute to both fasting and postprandial hyperglycemia. This may involve stimulation by GIP, but evidence also points to a role of circulating amino acids, which are elevated due to steatosis-induced impaired glucagon-mediated hepatic clearance, in line with recent work suggesting that the alpha cells and the liver are linked in a close, amino acid-mediated feedback circuit. Thus, the gut plays an important role in the development of T2DM spurred by overeating and defective beta cells.

Original languageEnglish
JournalMetabolic Syndrome and Related Disorders
Volume15
Issue number6
Pages (from-to)259-262
Number of pages4
ISSN1540-4196
DOIs
Publication statusPublished - Aug 2017

    Research areas

  • Journal Article

ID: 52666799