title: Acute and long-term effects of Roux-en-Y gastric bypass on glucose metabolism in subjects with Type 2 diabetes and normal glucose tolerance.
abstract: Our aim was to study the potential mechanisms responsible for the improvement in glucose control in Type 2 diabetes (T2D) within days after Roux-en-Y gastric bypass (RYGB). Thirteen obese subjects with T2D and twelve matched subjects with normal glucose tolerance (NGT) were examined during a liquid meal before (Pre), 1 wk, 3 mo, and 1 yr after RYGB. Glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), glucose-dependent-insulinotropic polypeptide (GIP), and glucagon concentrations were measured. Insulin resistance (HOMA-IR), β-cell glucose sensitivity (β-GS), and disposition index (D(β-GS): β-GS × 1/HOMA-IR) were calculated. Within the first week after RYGB, fasting glucose [T2D Pre: 8.8 ± 2.3, 1 wk: 7.0 ± 1.2 (P < 0.001)], and insulin concentrations decreased significantly in both groups. At 129 min, glucose concentrations decreased in T2D [Pre: 11.4 ± 3, 1 wk: 8.2 ± 2 (P = 0.003)] but not in NGT. HOMA-IR decreased by 50% in both groups. β-GS increased in T2D [Pre: 1.03 ± 0.49, 1 wk: 1.70 ± 1.2, (P = 0.012)] but did not change in NGT. The increase in DI(β-GS) was 3-fold in T2D and 1.5-fold in NGT. After RYGB, glucagon secretion was increased in response to the meal. GIP secretion was unchanged, while GLP-1 secretion increased more than 10-fold in both groups. The changes induced by RYGB were sustained or further enhanced 3 mo and 1 yr after surgery. Improvement in glycemic control in T2D after RYGB occurs within days after surgery and is associated with increased insulin sensitivity and improved β-cell function, the latter of which may be explained by dramatic increases in GLP-1 secretion.
authors.affiliation: Department of Endocrinology, Hvidovre Hospital, Hvidovre, Denmark. nils.bruun.joergensen@gmail.com
authors.forename: N B
authors.initials: NB
authors.lastname: Jørgensen
authors.forename: S H
authors.initials: SH
authors.lastname: Jacobsen
authors.forename: C
authors.initials: C
authors.lastname: Dirksen
authors.forename: K N
authors.initials: KN
authors.lastname: Bojsen-Møller
authors.forename: L
authors.initials: L
authors.lastname: Naver
authors.forename: L
authors.initials: L
authors.lastname: Hvolris
authors.forename: T R
authors.initials: TR
authors.lastname: Clausen
authors.forename: B S
authors.initials: BS
authors.lastname: Wulff
authors.forename: D
authors.initials: D
authors.lastname: Worm
authors.forename: D
authors.initials: D
authors.lastname: Lindqvist Hansen
authors.forename: S
authors.initials: S
authors.lastname: Madsbad
authors.forename: J J
authors.initials: JJ
authors.lastname: Holst
mesh_terms: D000328:Adult; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D005260:Female; D005500:Follow-Up Studies; D015390:Gastric Bypass; D005934:Glucagon / Q000097:blood / Q000378:metabolism; D052216:Glucagon-Like Peptide 1 / Q000097:blood / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000517:prevention & control; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology / Q000601:surgery*; D009767:Obesity, Morbid / Q000150:complications / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery; D019518:Postprandial Period; D013997:Time Factors
chemical_list: D002096:C-Peptide; D052216:Glucagon-Like Peptide 1; D005934:Glucagon; D005947:Glucose