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- Title
Putting the Hindgut Hypothesis to the Test in a Diabetic Zucker Rat Model.
- Authors
Laessle, Claudia; Jin, Ke; Seifert, Gabriel J; Timme-Bronsert, Sylvia; Fichtner-Feigl, Stefan; Marjanovic, Goran; Fink, Jodok Matthias
- Abstract
Background: The hindgut theory hypothesizes a key role of differential hindgut stimulation following metabolic procedures in ameliorating diabetes mellitus. We used two strategies to remove the hindgut from intestinal continuity in order to analyze its impact on diabetes mellitus. Methods: Loop duodeno-jejunostomy (DJOS) with exclusion of one-third of total intestinal length was performed in 3 groups of 9-week-old Zucker diabetic fatty rats. In group 1, no further alteration of the intestinal tract was made. Group 2 received additional ileal exclusion (IE). Group 3 underwent additional resection of 50% of the ileum with side-to-side ileocecal anastomosis (IR). One, 2, and 4 months after surgery, fasting blood glucose levels, oral glucose tolerance tests (OGTT), and glucose-stimulated hormone analyses were conducted, and bile acid blood levels were compared. Body weight was documented weekly. Results: In relation to DJOS, glucose control was not impaired in IR or IE. On the contrary, only IR could maintain preOP glucose values until 4 months. There were no significant weight differences between the groups. Confirming effective ileal diversion, bile acid blood levels were significantly higher in the DJOS group compared with both IR and IE (p = 0.0025 and p = 0.0047). Operative interventions had no impact on GLP-1 levels at any time point (ANOVA p > 0.05 for all). Insulin secretion was preserved in all groups. Conclusion: This data supports the hypothesis that the mechanisms driving amelioration of diabetes mellitus are complex and cannot be reduced to the ileum.
- Subjects
GLUCOSE tolerance tests; BLOOD sugar; ILEAL conduit surgery; DIABETES; RATS; BILE acids
- Publication
Obesity Surgery, 2019, Vol 29, Issue 12, p4000
- ISSN
0960-8923
- Publication type
Article
- DOI
10.1007/s11695-019-04079-w