WBR0808

Author	[[PageAuthor::Yazan Daaboul, M.D. (Reviewed by Serge Korjian)]]
Exam Type	ExamType::USMLE Step 1
Main Category	MainCategory::Physiology
Sub Category	SubCategory::Gastrointestinal
Prompt	[[Prompt::A researcher is studying the effect of a novel gastric inhibitory peptide (GIP) analog, GIP42, in mice. He follows the plasma concentration of compound X following the oral intake of GIP42 in experiment 1 and following intravenous (I.V.) administration of GIP42 in experiment 2. The graph below demonstrates the evolution of plasma concentrations of compound X during both experiments. Based on the researcher's findings, compound X most likely corresponds to which endogenous compound? ]]
Answer A	AnswerA::Glucagon
Answer A Explanation	AnswerAExp::GIP induces the secretion of insulin, not glucagon. GIP, glucagon, and secretin belong to the same family of hormones.
Answer B	AnswerB::Insulin
Answer B Explanation	AnswerBExp::GIP secretion within the GI tract induces insulin secretion in a phenomenon called "incretin effect".
Answer C	AnswerC::Motilin
Answer C Explanation	AnswerCExp::A distinct relation between motilin and GIP is not established.
Answer D	AnswerD::Secretin
Answer D Explanation	AnswerDExp::The main "incretin effect" is seen in insulin following GIP intake, not in secretin. GIP, glucagon, and secretin belong to the same family of hormones.
Answer E	AnswerE::Hydrogen ions
Answer E Explanation	[[AnswerEExp::GIP inhibits the release of H+.]]
Right Answer	RightAnswer::B
Explanation	[[Explanation::Gastric inhibitory peptide (GIP), also known as glucose-dependent insulinotropic peptide is a GI hormone secreted by K cells in the duodenum and the jejunum. GIP is considered an incretin, i.e. a molecule that increases the amount of insulin released from pancreatic beta cells of the islets of Langerhans. As such, oral GIP secretion following the oral intake of fatty acid, amino acids, and glucose, leads to an "incretin effect" due to the increased secretion of insulin following release of GIP in the GI tract. The elevation in insulin levels is not seen in I.V. infusion of GIP. As a result, "incretin effect" is seen following oral GIP but not I.V. GIP, which explains the variation in plasma concentration of compound X (insulin) during each experiment. In addition to GIP, another incretin is GLP-1 (glucagon-like peptide-1) hormone. Both incretins migrate in the circulation to the beta cells of the pancreas, their target cells to stimulate insulin secretion. It has been postulated the incretin effect is defective in type 2 diabetes mellitus (T2DM); GLP-1 analogs are currently pharmacologic options for patients with T2DM. Educational Objective: Oral GIP intake or GIP secretion within the GI tract following a meal induces insulin secretion in a phenomenon called "incretin effect". References: Martin JH, Deacon CF, Gorrell MD, Prins JB. Incretin-based therapies - review of the physiology, pharmacology and emerging clinical experience. Intern Med J. 2011;41(4):299-307.]]
Approved	Approved::Yes
Keyword	WBRKeyword::Insulin, WBRKeyword::Incretin effect, WBRKeyword::Incretins, WBRKeyword::GLP-1, WBRKeyword::GLP, WBRKeyword::GIP, WBRKeyword::Gastric inhibitory peptide, WBRKeyword::Hormone, WBRKeyword::Glucagon, WBRKeyword::Secretin, WBRKeyword::Diabetes, WBRKeyword::Type 2 diabetes mellitus
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