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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EIn the 44th Claude Bernard Lecture on diabetes, Daniel J. Drucker, MD, University of Toronto, Toronto, Ontario, Canada, discussed his research findings concerning incretin hormone action and the treatment of diabetes. The lecture covered the pharmacological\/physiological mechanisms of the glucagon-like peptides GLP-1 and GLP-2, and their relevance to the treatment of human disease.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EInfectious Disease\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EHormone Therapy\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EDiabetes Mellitus Diabetes \u0026amp; Metabolic Syndrome\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EIn the 44th Claude Bernard Lecture on diabetes, Daniel J. Drucker, MD, University of Toronto, Toronto, Ontario, Canada, discussed his research findings concerning incretin hormone action and the treatment of diabetes. The lecture covered the pharmacological\/physiological mechanisms of the glucagon-like peptides GLP-1 and GLP-2, and their relevance to the treatment of human disease.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EThe importance of GLP-1 system basal control of glucose homeostasis was first evidenced in animal studies in which GLP-1 receptor (GLP-1R) knockout (\u2212\/\u2212) mice exhibited increases in fasting blood glucose and decreases in circulating insulin following oral and intraperitoneal glucose challenges [Scrocchi LA et al. \u003Cem\u003ENat Med\u003C\/em\u003E 1996]. Since then, numerous studies have shown that the GLP-1\/GLP-1R system, although classically focused on the \u03b2-cell, is also critically important for the physiology of many other systems (eg, energy expenditure, central nervous system stress response, and the immune system).\u003C\/p\u003E\u003Cp id=\u0022p-4\u0022\u003EGiven that glucagon is a critical hormone in the pathophysiology of diabetes and the control of glucose homeostasis, can hyperglucagonemia of type 2 diabetes mellitus (T2DM) be attenuated successfully and used as a treatment for diabetes? One concern is whether blocking the glucagon receptor (Gcgr) is the right approach. GLP-1 and GLP-2 play key roles in cell proliferation and survival, and it is possible that the Gcgr may have a similar function that would make blocking it a poor choice for T2DM therapy.\u003C\/p\u003E\u003Cp id=\u0022p-5\u0022\u003EGcgr\u2212\/\u2212 mice have shown that the Gcgr is required for control of lipid metabolism during the adaptive metabolic response to fasting. Glucagon inhibits hepatic lipid production and acutely increases hepatic lipid secretion. Fasting Gcgr\u2212\/\u2212 mice are unable to control plasma lipids and experience an increase in triglyceride secretion from the liver. These mice are also resistant to diet-induced obesity and fat deposition in peripheral organs; however, they do not resist lipid deposition in the liver, somewhat negating any therapeutic potential [Longuet C et al. \u003Cem\u003ECell Metab\u003C\/em\u003E 2008]. Gcgr\u2212\/\u2212 mice also show enhanced susceptibility to hepatosteatosis on a methionine choline-deficient diet. Restoration of hepatic Gcgr expression attenuates the development of hepatocellular injury, which extends the essential actions of the Gcgr beyond the metabolic control of glucose homeostasis to encompass the regulation of hepatocyte survival [Sinclair EM et al. \u003Cem\u003EGastroenterology\u003C\/em\u003E 2008]. Independent of the lipid pathway, Gcgr plays a critical role in the balance between survival and cell death by way of lipid oxidation control. During fasting, increases in many of the genes in the liver important for liver oxidation are seen, but Gcgr\u2212\/\u2212 mice are unable to activate similar hepatic gene expression systems (\u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E) [Longuet C et al. \u003Cem\u003ECell Metab\u003C\/em\u003E 2008]. Thus, glucagon actions in the liver are essential for both hepatocyte survival and lipid accumulation.\u003C\/p\u003E\u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/16\/6\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Ggcr Signaling Is Essential for Control of Hepatic Lipid Oxidation.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1080479451\u0022 data-figure-caption=\u0022Ggcr Signaling Is Essential for Control of Hepatic Lipid Oxidation.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/16\/6\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/16\/6\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/16\/6\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/13078\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n            \u003Cp id=\u0022p-6\u0022 class=\u0022first-child\u0022\u003EGgcr Signaling Is Essential for Control of Hepatic Lipid Oxidation.\u003C\/p\u003E\n         \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003E* p\u0026lt;0.05; ** p \u0026lt; 0.01; *** p\u0026lt;0.001. KO=knockout; WT=wild-type. Reprinted from Longuet C et al. The Glucagon Receptor Is Required for the Adaptive Metabolic Response to Fasting. \u003Cem\u003ECell Metab\u003C\/em\u003E Nov 5, 2008;8(5):359\u2013371, with permission from Elsevier.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cp id=\u0022p-7\u0022\u003EGcgr also plays an important role in the pancreas in that Gcgr\u2212\/\u2212 mice have increased pancreatic weight, enhanced \u03b2-cell function, and massive islet and \u03b1-cell hyperplasia. Reductions in Gcgr signaling direct the pancreas to enhance islet \u03b1-cell proliferation, which develops independently of GLP-1R in Gcgr\u2212\/\u2212 mice [Ali S et al. \u003Cem\u003EJ Clin Invest\u003C\/em\u003E 2011]. The liver sends the signal to \u03b2-cells to proliferate; in control experiments genetic disruption of liver Gcgr sends a signal promoting proliferation of transplanted wild-type (WT) \u03b1-cells under the kidney capsule. But \u03b1-cell hyperplasia and proliferation can still occur very rapidly if WT islets are placed under the kidney capsule in mice with liver-selective inactivation of Gcgr. Thus, organized nerves, \u03b1-cells within the islets, or even islet cells organized within their normal location are not needed for this signal to be communicated [Longuet C et al. \u003Cem\u003EDiabetes.\u003C\/em\u003E In press]. The importance of liver Gcgr to the \u03b1-cell axis has also been shown in humans. In a recent clinical study the Gcgr antagonist MK-0893 produced robust reductions in HbA1C levels in patients with T2DM [Engel SS et al. ADA 2011 Abstract 309-OR] but was associated with elevations in transaminase and lipids.\u003C\/p\u003E\u003Cp id=\u0022p-8\u0022\u003EThe attenuation of Gcgr signaling produces substantial improvement of glucose homeostasis in mice and humans. This signaling is essential for hepatocyte survival, lipid metabolism, and controlling the rate of \u03b1-cell proliferation\u2014likely through a circulating factor.\u003C\/p\u003E\u003Cp id=\u0022p-9\u0022\u003EHowever, the therapeutic window for reduction of glucagon action to manifest beneficial effects for glucose control while avoiding enhancement of hepatic lipid storage, dyslipidemia, hepatocyte injury, and \u03b1-cell proliferation in diabetic subjects is unclear.\u003C\/p\u003E\u003Cp id=\u0022p-10\u0022\u003ETwo classes of medication that enhance incretin action (the GLP-1R agonists and dipeptidyl peptidase-4 [DPP-4] inhibitors) are used to treat T2DM. Prof. Drucker discussed the cardiovascular biology of these medications, including their direct and indirect effects on cardiomyocytes, blood vessels, adipocytes, blood pressure control, and postprandial lipoprotein secretion.\u003C\/p\u003E\u003Cp id=\u0022p-11\u0022\u003EWhen the mesenteric arteries of WT and Glp1r\u2212\/\u2212 mice were treated with GLP-1, GLP-1 (9\u201336), and exendin-4 (a GLP-1 agonist), GLP-1 and GLP-1 (9\u201336) exerted direct vasodilatory effects but exendin-4 did not. When the degradation of native GLP-1 is blocked by the addition of a DPP-4 inhibitor, vasodilation is substantially reduced but not completely eliminated in either group. This is likely because GLP-1 (9\u201336), a more potent vasodilator than GLP-1, was acting directly on the blood vessel [Ban K et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2008]. It has been suggested that there are GLP-1 receptors on endothelial or smooth muscle cells. However, in preconstricted mouse arteries the degradation-resistant GLP-1R agonist liraglutide does not directly vasodilate these arteries, but acetylcholine does. Support for the hypothesis that there is no direct action on blood vessels for these GLP-1R agonists comes from a recent clinical trial that showed exenatide BID for 3 months had no effect on microvascular endothelial function in obese, nondiabetic subjects [Kelly AS et al. \u003Cem\u003ECardiovasc\u003C\/em\u003E 2012]. In the cardiovascular system, pretreatment with liraglutide before coronary artery occlusion in normal and diabetic mice improved survival, reduced cardiac rupture and infarct size, and improved cardiac output. Liraglutide also modulated the expression and activity of cardioprotective genes in the mouse heart in a GLP-1R-dependent manner [Noyan-Ashraf MH et al. \u003Cem\u003EDiabetes\u003C\/em\u003E 2009].\u003C\/p\u003E\u003Cp id=\u0022p-12\u0022\u003EGLP-1R is expressed in the cardiovascular system in the heart and blood vessels, and, although activation of the GLP-1R is cardioprotective, the mechanisms by which this occurs are poorly understood and most likely the result of both direct and indirect action. Activation of GLP-1R also modulates inflammation; however, GLP-1R is not expressed in most mouse macrophage populations and further analyses requires a more stringent methodology.\u003C\/p\u003E\u003Cp id=\u0022p-13\u0022\u003EGLP-1 is synthesized in the enteroendocrine L cells and in the islet \u03b1-cells in the pancreas; however, nutrients increase L cell GLP-1 secretion and proglucagon-derived peptide biosynthesis but decrease glucagon biosynthesis and secretion in the islet \u03b1-cell. The molecular basis for this differential biology can be detected in the gene expression profiling of these two entities. Progesterone (P4) is an unexpected modulator of GLP-1 secretion in mice: enteral P4 increases plasma levels of GLP-1 and enhances glucose tolerance independent of the classical progesterone. The membrane progesterone receptors Paqr5 and Paqr7 are expressed in the gastrointestinal tract and in gut endocrine cell lines, and are essential for P4-mediatged GLP-1 secretion in GLUTag cells. Gut-restricted Paqr5 and Paqr7 agonists may enhance incretin secretion and control glucose homeostasis without systemic absorption of the ligands.\u003C\/p\u003E\u003Cp id=\u0022p-14\u0022\u003EGLP-2, a 33-aa peptide, stimulates crypt cell proliferation and produces a marked increase in bowel weight and villus growth of the jejunum and ileum. Glp2r-\/- mice exhibit enhanced sensitivity to nonsteroidal anti-inflammatory drug-induced gut injury and abnormal host-bacterial interactions [Lee SJ et al. \u003Cem\u003EEndocrinology\u003C\/em\u003E 2012]. GLP-2 also has a role in the control of nutrient absorption. GLP-2 rapidly enhances intestinal blood flow; increases the absorption of sugars, proteins, and fats; reduces acid secretion; and delays gut motility. Teduglutide, a GLP-2 analogue, reduced volume and number of days of parenteral support for patients with short bowel syndrome, suggesting GLP-2 can restore nutritional balance and reduce parenteral nutrition requirements in these subjects (\u003Ca id=\u0022xref-fig-2-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F2\u0022\u003EFigure 2\u003C\/a\u003E) [Jeppesen PB et al. \u003Cem\u003EGastroenterology\u003C\/em\u003E 2012].\u003C\/p\u003E\u003Cdiv id=\u0022F2\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/16\/6\/F2.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Teduglutide Reduces Parenteral Nutrition Requirements in Human Subjects with Short Bowel Syndrome.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1080479451\u0022 data-figure-caption=\u0022Teduglutide Reduces Parenteral Nutrition Requirements in Human Subjects with Short Bowel Syndrome.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 2.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/16\/6\/F2.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/16\/6\/F2.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 2.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/16\/6\/F2.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/13080\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 2.\u003C\/span\u003E \n            \u003Cp id=\u0022p-15\u0022 class=\u0022first-child\u0022\u003ETeduglutide Reduces Parenteral Nutrition Requirements in Human Subjects with Short Bowel Syndrome.\u003C\/p\u003E\n         \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-2\u0022\u003EReprinted from Jeppesen PB et al. Teduglutide Reduces Need for Parenteral Support Among Patients With Short Bowel Syndrome With Intestinal Failure. \u003Cem\u003EGastroenterology\u003C\/em\u003E Jan 1, 2012; S0016\u20135085(12) 01316\u20139, with permission from Elsevier.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cp id=\u0022p-16\u0022\u003EGLP-1 has many intriguing effects on blood vessels and the heart that are of interest to clinicians. Prof. Drucker concluded by saying, \u201cWhat I\u0027ve tried to illustrate is that the techniques we use to detect GLP-1R expression either at the RNA [ribonucleic acid] level or protein level perhaps need a little bit more thought and rigor in terms of interpretation. And finally I\u0027ve tried to convince you that perhaps GLP-2\u2026may potentially be useful in the treatment of patients who have trouble with their own endogenous gut functions.\u201d Considerable progress has been made, but considering the number of patients with diabetes and the advanced technology available, there is still a lot of work to do in the treatment of patients with diabetes.\u003C\/p\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2012 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/12\/16\/6.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzn8hp\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzn8hp\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}