Type 2 Diabetes: An Overview
Type 2 diabetes is a heterogeneous disorder. Clinical expression of the disorder requires both genetic and environmental factors. One theory concerning its etiology is that it is the result of the evolution of a thrifty genotype that had survival benefits in the past but is detrimental in the curren...
Gespeichert in:
Veröffentlicht in: | Clinical chemistry (Baltimore, Md.) Md.), 1999-08, Vol.45 (8), p.1339-1345 |
---|---|
1. Verfasser: | |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 1345 |
---|---|
container_issue | 8 |
container_start_page | 1339 |
container_title | Clinical chemistry (Baltimore, Md.) |
container_volume | 45 |
creator | Lebovitz, Harold E |
description | Type 2 diabetes is a heterogeneous disorder. Clinical expression of the disorder requires both genetic and environmental factors. One theory concerning its etiology is that it is the result of the evolution of a thrifty genotype that had survival benefits in the past but is detrimental in the current environment. An opposing theory is that it represents an adult metabolic response to fetal malnutrition. Hyperglycemia in type 2 diabetes results from absolute or relative insulin deficiency. Most often relative insulin deficiency is attributable to an inability to adequately compensate for insulin resistance. Insulin resistance may be caused by a variety of genetic or metabolic factors. The most common etiological factor in insulin resistance is central obesity. Insulin resistance is associated with a cluster of metabolic abnormalities that include glucose intolerance, hypertension, a unique dyslipidemia, a procoagulant state, and an increase in macrovascular disease. Clinical intervention studies have demonstrated that reduction in the chronic microvascular and macrovascular complications of type 2 diabetes requires treatment of hyperglycemia to achieve hemoglobin A1c |
doi_str_mv | 10.1093/clinchem/45.8.1339 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69965643</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69965643</sourcerecordid><originalsourceid>FETCH-LOGICAL-c469t-28532b6a0ef3bb29a56d894a6bf3292ee41e1ddc65c9d308abad286dbca509303</originalsourceid><addsrcrecordid>eNpNkEtPAjEUhRujEUT_gDGGhXE30DetO4LPhIQNrpu2c0dqZgZsgQn_3iFgcHVzk--cc-9B6JbgAcGaDX0Zar-AasjFQA0IY_oMdYlgOFNCknPUxRjrTBM-6qCrlL7blY-UvEQdgjnDisguupvvVtCn_edgHawhPfXHdX-2hbgN0Fyji8KWCW6Os4c-X1_mk_dsOnv7mIynmedSrzOqBKNOWgwFc45qK2SuNLfSFYxqCsAJkDz3Unidt7nW2ZwqmTtvRfsHZj30ePBdxeXPBtLaVCF5KEtbw3KTjNRaCslZC9ID6OMypQiFWcVQ2bgzBJt9J-avE8OFUWbfSSu6P7pvXAX5P8mhhBZ4OAI2eVsW0dY-pBOnJVNCna5chK9FEyKYVNmybF2JaZrmFPgLLdt27g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>69965643</pqid></control><display><type>article</type><title>Type 2 Diabetes: An Overview</title><source>Oxford University Press Journals</source><source>MEDLINE</source><creator>Lebovitz, Harold E</creator><creatorcontrib>Lebovitz, Harold E</creatorcontrib><description>Type 2 diabetes is a heterogeneous disorder. Clinical expression of the disorder requires both genetic and environmental factors. One theory concerning its etiology is that it is the result of the evolution of a thrifty genotype that had survival benefits in the past but is detrimental in the current environment. An opposing theory is that it represents an adult metabolic response to fetal malnutrition. Hyperglycemia in type 2 diabetes results from absolute or relative insulin deficiency. Most often relative insulin deficiency is attributable to an inability to adequately compensate for insulin resistance. Insulin resistance may be caused by a variety of genetic or metabolic factors. The most common etiological factor in insulin resistance is central obesity. Insulin resistance is associated with a cluster of metabolic abnormalities that include glucose intolerance, hypertension, a unique dyslipidemia, a procoagulant state, and an increase in macrovascular disease. Clinical intervention studies have demonstrated that reduction in the chronic microvascular and macrovascular complications of type 2 diabetes requires treatment of hyperglycemia to achieve hemoglobin A1c <7.0%, blood pressure </=130/80 mmHg, and plasma LDL-cholesterol </=2.6 mmol/L (</=100 mg/dL). Oral antihyperglycemic agents increase endogenous insulin secretion, decrease insulin resistance, or lower postprandial plasma glucose rise by delaying absorption of complex carbohydrates. Long-term glycemic control in type 2 diabetes requires progressive, stepwise, combination treatment with oral agents and eventually combination treatment with oral agents and insulin.</description><identifier>ISSN: 0009-9147</identifier><identifier>EISSN: 1530-8561</identifier><identifier>DOI: 10.1093/clinchem/45.8.1339</identifier><identifier>PMID: 10430816</identifier><identifier>CODEN: CLCHAU</identifier><language>eng</language><publisher>Washington, DC: Am Assoc Clin Chem</publisher><subject>Biological and medical sciences ; Cardiovascular Diseases - prevention & control ; Diabetes Mellitus, Type 2 - classification ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - etiology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Humans ; Hypoglycemic Agents - therapeutic use ; Insulin Resistance ; Medical sciences ; Obesity - etiology ; Risk Factors</subject><ispartof>Clinical chemistry (Baltimore, Md.), 1999-08, Vol.45 (8), p.1339-1345</ispartof><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-28532b6a0ef3bb29a56d894a6bf3292ee41e1ddc65c9d308abad286dbca509303</citedby><cites>FETCH-LOGICAL-c469t-28532b6a0ef3bb29a56d894a6bf3292ee41e1ddc65c9d308abad286dbca509303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,23921,23922,25131,27915,27916</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1963858$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10430816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lebovitz, Harold E</creatorcontrib><title>Type 2 Diabetes: An Overview</title><title>Clinical chemistry (Baltimore, Md.)</title><addtitle>Clin Chem</addtitle><description>Type 2 diabetes is a heterogeneous disorder. Clinical expression of the disorder requires both genetic and environmental factors. One theory concerning its etiology is that it is the result of the evolution of a thrifty genotype that had survival benefits in the past but is detrimental in the current environment. An opposing theory is that it represents an adult metabolic response to fetal malnutrition. Hyperglycemia in type 2 diabetes results from absolute or relative insulin deficiency. Most often relative insulin deficiency is attributable to an inability to adequately compensate for insulin resistance. Insulin resistance may be caused by a variety of genetic or metabolic factors. The most common etiological factor in insulin resistance is central obesity. Insulin resistance is associated with a cluster of metabolic abnormalities that include glucose intolerance, hypertension, a unique dyslipidemia, a procoagulant state, and an increase in macrovascular disease. Clinical intervention studies have demonstrated that reduction in the chronic microvascular and macrovascular complications of type 2 diabetes requires treatment of hyperglycemia to achieve hemoglobin A1c <7.0%, blood pressure </=130/80 mmHg, and plasma LDL-cholesterol </=2.6 mmol/L (</=100 mg/dL). Oral antihyperglycemic agents increase endogenous insulin secretion, decrease insulin resistance, or lower postprandial plasma glucose rise by delaying absorption of complex carbohydrates. Long-term glycemic control in type 2 diabetes requires progressive, stepwise, combination treatment with oral agents and eventually combination treatment with oral agents and insulin.</description><subject>Biological and medical sciences</subject><subject>Cardiovascular Diseases - prevention & control</subject><subject>Diabetes Mellitus, Type 2 - classification</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - etiology</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>Humans</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Insulin Resistance</subject><subject>Medical sciences</subject><subject>Obesity - etiology</subject><subject>Risk Factors</subject><issn>0009-9147</issn><issn>1530-8561</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkEtPAjEUhRujEUT_gDGGhXE30DetO4LPhIQNrpu2c0dqZgZsgQn_3iFgcHVzk--cc-9B6JbgAcGaDX0Zar-AasjFQA0IY_oMdYlgOFNCknPUxRjrTBM-6qCrlL7blY-UvEQdgjnDisguupvvVtCn_edgHawhPfXHdX-2hbgN0Fyji8KWCW6Os4c-X1_mk_dsOnv7mIynmedSrzOqBKNOWgwFc45qK2SuNLfSFYxqCsAJkDz3Unidt7nW2ZwqmTtvRfsHZj30ePBdxeXPBtLaVCF5KEtbw3KTjNRaCslZC9ID6OMypQiFWcVQ2bgzBJt9J-avE8OFUWbfSSu6P7pvXAX5P8mhhBZ4OAI2eVsW0dY-pBOnJVNCna5chK9FEyKYVNmybF2JaZrmFPgLLdt27g</recordid><startdate>19990801</startdate><enddate>19990801</enddate><creator>Lebovitz, Harold E</creator><general>Am Assoc Clin Chem</general><general>American Association for Clinical Chemistry</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>19990801</creationdate><title>Type 2 Diabetes: An Overview</title><author>Lebovitz, Harold E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-28532b6a0ef3bb29a56d894a6bf3292ee41e1ddc65c9d308abad286dbca509303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Biological and medical sciences</topic><topic>Cardiovascular Diseases - prevention & control</topic><topic>Diabetes Mellitus, Type 2 - classification</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - etiology</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>Humans</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Insulin Resistance</topic><topic>Medical sciences</topic><topic>Obesity - etiology</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lebovitz, Harold E</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>Clinical chemistry (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lebovitz, Harold E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Type 2 Diabetes: An Overview</atitle><jtitle>Clinical chemistry (Baltimore, Md.)</jtitle><addtitle>Clin Chem</addtitle><date>1999-08-01</date><risdate>1999</risdate><volume>45</volume><issue>8</issue><spage>1339</spage><epage>1345</epage><pages>1339-1345</pages><issn>0009-9147</issn><eissn>1530-8561</eissn><coden>CLCHAU</coden><abstract>Type 2 diabetes is a heterogeneous disorder. Clinical expression of the disorder requires both genetic and environmental factors. One theory concerning its etiology is that it is the result of the evolution of a thrifty genotype that had survival benefits in the past but is detrimental in the current environment. An opposing theory is that it represents an adult metabolic response to fetal malnutrition. Hyperglycemia in type 2 diabetes results from absolute or relative insulin deficiency. Most often relative insulin deficiency is attributable to an inability to adequately compensate for insulin resistance. Insulin resistance may be caused by a variety of genetic or metabolic factors. The most common etiological factor in insulin resistance is central obesity. Insulin resistance is associated with a cluster of metabolic abnormalities that include glucose intolerance, hypertension, a unique dyslipidemia, a procoagulant state, and an increase in macrovascular disease. Clinical intervention studies have demonstrated that reduction in the chronic microvascular and macrovascular complications of type 2 diabetes requires treatment of hyperglycemia to achieve hemoglobin A1c <7.0%, blood pressure </=130/80 mmHg, and plasma LDL-cholesterol </=2.6 mmol/L (</=100 mg/dL). Oral antihyperglycemic agents increase endogenous insulin secretion, decrease insulin resistance, or lower postprandial plasma glucose rise by delaying absorption of complex carbohydrates. Long-term glycemic control in type 2 diabetes requires progressive, stepwise, combination treatment with oral agents and eventually combination treatment with oral agents and insulin.</abstract><cop>Washington, DC</cop><pub>Am Assoc Clin Chem</pub><pmid>10430816</pmid><doi>10.1093/clinchem/45.8.1339</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0009-9147 |
ispartof | Clinical chemistry (Baltimore, Md.), 1999-08, Vol.45 (8), p.1339-1345 |
issn | 0009-9147 1530-8561 |
language | eng |
recordid | cdi_proquest_miscellaneous_69965643 |
source | Oxford University Press Journals; MEDLINE |
subjects | Biological and medical sciences Cardiovascular Diseases - prevention & control Diabetes Mellitus, Type 2 - classification Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - etiology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Humans Hypoglycemic Agents - therapeutic use Insulin Resistance Medical sciences Obesity - etiology Risk Factors |
title | Type 2 Diabetes: An Overview |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T19%3A03%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Type%202%20Diabetes:%20An%20Overview&rft.jtitle=Clinical%20chemistry%20(Baltimore,%20Md.)&rft.au=Lebovitz,%20Harold%20E&rft.date=1999-08-01&rft.volume=45&rft.issue=8&rft.spage=1339&rft.epage=1345&rft.pages=1339-1345&rft.issn=0009-9147&rft.eissn=1530-8561&rft.coden=CLCHAU&rft_id=info:doi/10.1093/clinchem/45.8.1339&rft_dat=%3Cproquest_cross%3E69965643%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=69965643&rft_id=info:pmid/10430816&rfr_iscdi=true |