Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass

Research output: Contribution to journalJournal articleResearchpeer-review

  1. Gut microbiota profile and selected plasma metabolites in type 1 diabetes without and with stratification by albuminuria

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Major decreases in the lipidome following liraglutide treatment: 21-25 September 2020.

    Research output: Contribution to journalConference abstract in journalResearchpeer-review

  1. The renal extraction and the natriuretic action of GLP-1 in humans depend on interaction with the GLP-1 receptor

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Counterregulatory responses to postprandial hypoglycemia after Roux-en-Y gastric bypass

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Fractionated free fatty acids and their relation to diabetes status after Roux-en-Y gastric bypass: A cohort study

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. Gut Mucosal Gene Expression and Metabolic Changes After Roux-en-Y Gastric Bypass Surgery

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations
Roux-en-Y gastric bypass (RYGB) greatly improves glycaemic control in morbidly obese patients with type 2 diabetes, in many even before significant weight loss. Understanding the responsible mechanisms may contribute to our knowledge of the pathophysiology of type 2 diabetes and help identify new drug targets or improve surgical techniques. This review summarises the present knowledge based on pathophysiological studies published during the last decade. Taken together, two main mechanisms seem to be responsible for the early improvement in glycaemic control after RYGB: (1) an increase in hepatic insulin sensitivity induced, at least in part, by energy restriction and (2) improved beta cell function associated with an exaggerated postprandial glucagon-like peptide 1 secretion owing to the altered transit of nutrients. Later a weight loss induced improvement in peripheral insulin sensitivity follows.
Original languageEnglish
JournalDiabetologia
Volume55
Issue number7
Pages (from-to)1890-901
Number of pages12
ISSN0012-186X
DOIs
Publication statusPublished - 2012

    Research areas

  • Blood Glucose, Diabetes Mellitus, Type 2, Female, Gastric Bypass, Glucagon-Like Peptide 1, Glucose Tolerance Test, Humans, Insulin Resistance, Insulin-Secreting Cells, Male, Obesity, Morbid, Time Factors, Treatment Outcome

ID: 36754171