Gastric Inhibitory Polypeptide: the neglected incretin revisited
After the ingestion of fat- and glucose-rich meals, gut hormones are secreted into the circulation in order to stimulate insulin secretion. This so-called “incretin effect” is primarily conferred by Glucagon-like peptide 1 (GLP-1) and Gastric Inhibitory Polypeptide (GIP). In contrast to GLP-1, GIP h...
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description | After the ingestion of fat- and glucose-rich meals, gut hormones are secreted into the circulation in order to stimulate insulin secretion. This so-called “incretin effect” is primarily conferred by Glucagon-like peptide 1 (GLP-1) and Gastric Inhibitory Polypeptide (GIP). In contrast to GLP-1, GIP has lost most of its insulinotropic effect in type 2 diabetic patients. In addition to its main physiological role in the regulation of endocrine pancreatic secretion, GIP exerts various peripheral effects on adipose tissue and lipid metabolism, thereby leading to increased lipid deposition in the postprandial state. In some animal models, an influence on gastrointestinal functions has been described. However, such effects do not seem to play an important role in humans. During the last years, the major line of research has focussed on GLP-1, due to its promising potential for the treatment of type 2 diabetes mellitus. However, the physiological importance of GIP in the regulation of insulin secretion has been shown to even exceed that of GLP-1. Furthermore, work from various groups has provided evidence that GIP contributes to the pathogenesis of type 2 diabetes to a considerable degree. Recent data with modified GIP analogues further suggested a possibility of therapeutic use in the treatment of type 2 diabetes. Thus, it seems worthwhile to refocus on this important and—sometimes—neglected incretin hormone. The present work aims to review the physiological functions of GIP, to characterize its role in the pathogenesis of type 2 diabetes, and to discuss possible clinical applications and future perspectives in the light of new findings. |
doi_str_mv | 10.1016/S0167-0115(02)00039-3 |
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This so-called “incretin effect” is primarily conferred by Glucagon-like peptide 1 (GLP-1) and Gastric Inhibitory Polypeptide (GIP). In contrast to GLP-1, GIP has lost most of its insulinotropic effect in type 2 diabetic patients. In addition to its main physiological role in the regulation of endocrine pancreatic secretion, GIP exerts various peripheral effects on adipose tissue and lipid metabolism, thereby leading to increased lipid deposition in the postprandial state. In some animal models, an influence on gastrointestinal functions has been described. However, such effects do not seem to play an important role in humans. During the last years, the major line of research has focussed on GLP-1, due to its promising potential for the treatment of type 2 diabetes mellitus. However, the physiological importance of GIP in the regulation of insulin secretion has been shown to even exceed that of GLP-1. Furthermore, work from various groups has provided evidence that GIP contributes to the pathogenesis of type 2 diabetes to a considerable degree. Recent data with modified GIP analogues further suggested a possibility of therapeutic use in the treatment of type 2 diabetes. Thus, it seems worthwhile to refocus on this important and—sometimes—neglected incretin hormone. The present work aims to review the physiological functions of GIP, to characterize its role in the pathogenesis of type 2 diabetes, and to discuss possible clinical applications and future perspectives in the light of new findings.</description><identifier>ISSN: 0167-0115</identifier><identifier>EISSN: 1873-1686</identifier><identifier>DOI: 10.1016/S0167-0115(02)00039-3</identifier><identifier>PMID: 12137960</identifier><identifier>CODEN: REPPDY</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>Adipose Tissue - drug effects ; Adipose Tissue - physiology ; Amino Acid Sequence ; Animals ; Biological and medical sciences ; Blood Glucose - analysis ; C-Peptide - blood ; Diabetes Mellitus, Type 2 - pathology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Gastric Inhibitory Polypeptide - metabolism ; Gastric Inhibitory Polypeptide - pharmacology ; Gastric Inhibitory Polypeptide - physiology ; Glucagon - metabolism ; Glucagon-Like Peptide 1 ; Glucose - metabolism ; Humans ; Incretin effect ; Insulin - blood ; Insulin secretion ; Lipids - physiology ; Medical sciences ; Models, Biological ; Molecular Sequence Data ; Pancreatic Hormones - metabolism ; Pathogenesis of type 2 diabetes ; Peptide Fragments - metabolism ; Postprandial Period ; Protein Precursors - metabolism ; Secretin - pharmacology ; Sequence Homology, Amino Acid ; Stomach - drug effects ; Stomach - physiology ; Treatment of type 2 diabetes</subject><ispartof>Regulatory Peptides, 2002-07, Vol.107 (1), p.1-13</ispartof><rights>2002 Elsevier Science B.V.</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-6237ad2796fb1abac820ec0edd76e5827dd60ccf30e88191550534250eefa0643</citedby><cites>FETCH-LOGICAL-c457t-6237ad2796fb1abac820ec0edd76e5827dd60ccf30e88191550534250eefa0643</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0167011502000393$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>313,314,776,780,788,3537,27899,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13824748$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12137960$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Meier, Juris J</creatorcontrib><creatorcontrib>Nauck, Michael A</creatorcontrib><creatorcontrib>Schmidt, Wolfgang E</creatorcontrib><creatorcontrib>Gallwitz, Baptist</creatorcontrib><title>Gastric Inhibitory Polypeptide: the neglected incretin revisited</title><title>Regulatory Peptides</title><addtitle>Regul Pept</addtitle><description>After the ingestion of fat- and glucose-rich meals, gut hormones are secreted into the circulation in order to stimulate insulin secretion. This so-called “incretin effect” is primarily conferred by Glucagon-like peptide 1 (GLP-1) and Gastric Inhibitory Polypeptide (GIP). In contrast to GLP-1, GIP has lost most of its insulinotropic effect in type 2 diabetic patients. In addition to its main physiological role in the regulation of endocrine pancreatic secretion, GIP exerts various peripheral effects on adipose tissue and lipid metabolism, thereby leading to increased lipid deposition in the postprandial state. In some animal models, an influence on gastrointestinal functions has been described. However, such effects do not seem to play an important role in humans. During the last years, the major line of research has focussed on GLP-1, due to its promising potential for the treatment of type 2 diabetes mellitus. However, the physiological importance of GIP in the regulation of insulin secretion has been shown to even exceed that of GLP-1. Furthermore, work from various groups has provided evidence that GIP contributes to the pathogenesis of type 2 diabetes to a considerable degree. Recent data with modified GIP analogues further suggested a possibility of therapeutic use in the treatment of type 2 diabetes. Thus, it seems worthwhile to refocus on this important and—sometimes—neglected incretin hormone. The present work aims to review the physiological functions of GIP, to characterize its role in the pathogenesis of type 2 diabetes, and to discuss possible clinical applications and future perspectives in the light of new findings.</description><subject>Adipose Tissue - drug effects</subject><subject>Adipose Tissue - physiology</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - analysis</subject><subject>C-Peptide - blood</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Gastric Inhibitory Polypeptide - metabolism</subject><subject>Gastric Inhibitory Polypeptide - pharmacology</subject><subject>Gastric Inhibitory Polypeptide - physiology</subject><subject>Glucagon - metabolism</subject><subject>Glucagon-Like Peptide 1</subject><subject>Glucose - metabolism</subject><subject>Humans</subject><subject>Incretin effect</subject><subject>Insulin - blood</subject><subject>Insulin secretion</subject><subject>Lipids - physiology</subject><subject>Medical sciences</subject><subject>Models, Biological</subject><subject>Molecular Sequence Data</subject><subject>Pancreatic Hormones - metabolism</subject><subject>Pathogenesis of type 2 diabetes</subject><subject>Peptide Fragments - metabolism</subject><subject>Postprandial Period</subject><subject>Protein Precursors - metabolism</subject><subject>Secretin - pharmacology</subject><subject>Sequence Homology, Amino Acid</subject><subject>Stomach - drug effects</subject><subject>Stomach - physiology</subject><subject>Treatment of type 2 diabetes</subject><issn>0167-0115</issn><issn>1873-1686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkN9LwzAQx4Mobv74E5S-KPpQvSRN0_qiMnQOBgrqc8iSq4t07Uy6wf57u624R1_u4Ph8744PIWcUbijQ9Pa9LTIGSsUVsGsA4HnM90ifZpLHNM3SfdL_Q3rkKIRvACqk5IekRxnlMk-hTx6GOjTemWhUTd3ENbVfRW91uZrjvHEW76JmilGFXyWaBm3kKuOxcVXkcemCa0cn5KDQZcDTrh-Tz-enj8FLPH4djgaP49gkQjZxyrjUlrVHiwnVE20yBmgArZUpioxJa1MwpuCAWUZzKgQInjABiIWGNOHH5HK7d-7rnwWGRs1cMFiWusJ6EZSkeSJzxltQbEHj6xA8Fmru3Uz7laKg1urURp1ae1HA1EadWufOuwOLyQztLtW5aoGLDtDB6LLwujIu7DiesUQmWcvdbzlsdSwdehWMw8qgdb61qGzt_nnlFz7eil0</recordid><startdate>20020715</startdate><enddate>20020715</enddate><creator>Meier, Juris J</creator><creator>Nauck, Michael A</creator><creator>Schmidt, Wolfgang E</creator><creator>Gallwitz, Baptist</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20020715</creationdate><title>Gastric Inhibitory Polypeptide: the neglected incretin revisited</title><author>Meier, Juris J ; Nauck, Michael A ; Schmidt, Wolfgang E ; Gallwitz, Baptist</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-6237ad2796fb1abac820ec0edd76e5827dd60ccf30e88191550534250eefa0643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adipose Tissue - drug effects</topic><topic>Adipose Tissue - physiology</topic><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - analysis</topic><topic>C-Peptide - blood</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Gastric Inhibitory Polypeptide - metabolism</topic><topic>Gastric Inhibitory Polypeptide - pharmacology</topic><topic>Gastric Inhibitory Polypeptide - physiology</topic><topic>Glucagon - metabolism</topic><topic>Glucagon-Like Peptide 1</topic><topic>Glucose - metabolism</topic><topic>Humans</topic><topic>Incretin effect</topic><topic>Insulin - blood</topic><topic>Insulin secretion</topic><topic>Lipids - physiology</topic><topic>Medical sciences</topic><topic>Models, Biological</topic><topic>Molecular Sequence Data</topic><topic>Pancreatic Hormones - metabolism</topic><topic>Pathogenesis of type 2 diabetes</topic><topic>Peptide Fragments - metabolism</topic><topic>Postprandial Period</topic><topic>Protein Precursors - metabolism</topic><topic>Secretin - pharmacology</topic><topic>Sequence Homology, Amino Acid</topic><topic>Stomach - drug effects</topic><topic>Stomach - physiology</topic><topic>Treatment of type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meier, Juris J</creatorcontrib><creatorcontrib>Nauck, Michael A</creatorcontrib><creatorcontrib>Schmidt, Wolfgang E</creatorcontrib><creatorcontrib>Gallwitz, Baptist</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Regulatory Peptides</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Meier, Juris J</au><au>Nauck, Michael A</au><au>Schmidt, Wolfgang E</au><au>Gallwitz, Baptist</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gastric Inhibitory Polypeptide: the neglected incretin revisited</atitle><jtitle>Regulatory Peptides</jtitle><addtitle>Regul Pept</addtitle><date>2002-07-15</date><risdate>2002</risdate><volume>107</volume><issue>1</issue><spage>1</spage><epage>13</epage><pages>1-13</pages><issn>0167-0115</issn><eissn>1873-1686</eissn><coden>REPPDY</coden><abstract>After the ingestion of fat- and glucose-rich meals, gut hormones are secreted into the circulation in order to stimulate insulin secretion. This so-called “incretin effect” is primarily conferred by Glucagon-like peptide 1 (GLP-1) and Gastric Inhibitory Polypeptide (GIP). In contrast to GLP-1, GIP has lost most of its insulinotropic effect in type 2 diabetic patients. In addition to its main physiological role in the regulation of endocrine pancreatic secretion, GIP exerts various peripheral effects on adipose tissue and lipid metabolism, thereby leading to increased lipid deposition in the postprandial state. In some animal models, an influence on gastrointestinal functions has been described. However, such effects do not seem to play an important role in humans. During the last years, the major line of research has focussed on GLP-1, due to its promising potential for the treatment of type 2 diabetes mellitus. However, the physiological importance of GIP in the regulation of insulin secretion has been shown to even exceed that of GLP-1. Furthermore, work from various groups has provided evidence that GIP contributes to the pathogenesis of type 2 diabetes to a considerable degree. Recent data with modified GIP analogues further suggested a possibility of therapeutic use in the treatment of type 2 diabetes. Thus, it seems worthwhile to refocus on this important and—sometimes—neglected incretin hormone. The present work aims to review the physiological functions of GIP, to characterize its role in the pathogenesis of type 2 diabetes, and to discuss possible clinical applications and future perspectives in the light of new findings.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>12137960</pmid><doi>10.1016/S0167-0115(02)00039-3</doi><tpages>13</tpages></addata></record> |
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subjects | Adipose Tissue - drug effects Adipose Tissue - physiology Amino Acid Sequence Animals Biological and medical sciences Blood Glucose - analysis C-Peptide - blood Diabetes Mellitus, Type 2 - pathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Gastric Inhibitory Polypeptide - metabolism Gastric Inhibitory Polypeptide - pharmacology Gastric Inhibitory Polypeptide - physiology Glucagon - metabolism Glucagon-Like Peptide 1 Glucose - metabolism Humans Incretin effect Insulin - blood Insulin secretion Lipids - physiology Medical sciences Models, Biological Molecular Sequence Data Pancreatic Hormones - metabolism Pathogenesis of type 2 diabetes Peptide Fragments - metabolism Postprandial Period Protein Precursors - metabolism Secretin - pharmacology Sequence Homology, Amino Acid Stomach - drug effects Stomach - physiology Treatment of type 2 diabetes |
title | Gastric Inhibitory Polypeptide: the neglected incretin revisited |
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