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The stimulation of GIP secretion by lipid absorption – is it dose‐dependent?
Author(s) -
Yoder Stephanie,
Kindel Tammy,
Li Hui,
Xu Maggie,
Tso Patrick
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1184.1
Subject(s) - medicine , endocrinology , incretin , secretion , gastric inhibitory polypeptide , saline , ingestion , bolus (digestion) , stimulation , lymph , hormone , chemistry , glucagon , type 2 diabetes , diabetes mellitus , psychiatry
The incretin hormone glucose‐dependent insulinotropic polypeptide (GIP) enhances glucose‐mediated insulin secretion. Following nutrient ingestion, GIP secretion by enteroendocrine K cells increases rapidly. Previous studies have shown that fat ingestion stimulates GIP release; however, it is unknown if there is a dose‐dependent secretion of incretins to the ingestion of fat. We hypothesize that a direct dose‐dependent relationship exists between the amount of lipid infused and GIP secretion. To test this, lymph fistula rats were used. Under halothane anesthesia, the major mesenteric lymph duct was cannulated, and an infusion tube was placed in the duodenum. Each animal received a single bolus intraduodenally of saline or varying amounts of the fat emulsion Liposyn II. Lymph was continuously collected for 6 hours and analyzed for GIP content. At lipid doses of 27.5 and 55 mg, the secretion of GIP, over the 6 hour period, increased 1 fold above the saline control; at lipid doses of 110, 220, and 440 mg lipid, GIP secretion increased 2 fold above the control. Thus, our data suggest that GIP secretion increases incrementally rather than dose‐dependently in response to a larger lipid dose. Whether this paradigm will be altered in diet induced obese animals is a question of considerable interest to basic and clinical scientists. Funded by DK076928 ‐01A(NIH/NIDDK)