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Different β‐cell secretory phenotype in non‐obese compared to obese early type 2 diabetes
Background Type 2 diabetes (T2D) is characterized by impaired tissue sensitivity to insulin action (ie, insulin resistance) and impaired β‐cell insulin secretion. Because obesity contributes importantly to the development of insulin resistance, we sought to determine whether insulin secretory defect...
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| Published in: | Diabetes/metabolism research and reviews 2020-07, Vol.36 (5), p.e3295-n/a |
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| container_issue | 5 |
| container_start_page | e3295 |
| container_title | Diabetes/metabolism research and reviews |
| container_volume | 36 |
| creator | Gudipaty, Lalitha Rosenfeld, Nora K. Fuller, Carissa S. Cuchel, Marina Rickels, Michael R. |
| description | Background
Type 2 diabetes (T2D) is characterized by impaired tissue sensitivity to insulin action (ie, insulin resistance) and impaired β‐cell insulin secretion. Because obesity contributes importantly to the development of insulin resistance, we sought to determine whether insulin secretory defects would predominate in non‐obese compared to obese T2D.
Methods
We measured β‐cell function and secretory capacity using the glucose‐potentiated arginine test in T2D subjects early in the disease course classified as non‐obese (BMI |
| doi_str_mv | 10.1002/dmrr.3295 |
| format | article |
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Type 2 diabetes (T2D) is characterized by impaired tissue sensitivity to insulin action (ie, insulin resistance) and impaired β‐cell insulin secretion. Because obesity contributes importantly to the development of insulin resistance, we sought to determine whether insulin secretory defects would predominate in non‐obese compared to obese T2D.
Methods
We measured β‐cell function and secretory capacity using the glucose‐potentiated arginine test in T2D subjects early in the disease course classified as non‐obese (BMI <30; n = 12) or obese (BMI ≥30 kg/m2; n = 28) and additionally compared responses from non‐obese T2D with a non‐diabetic control group (n = 12).
Results
The acute insulin response to glucose potentiation of arginine‐induced insulin release was less in non‐obese T2D than in controls and associated with impaired β‐cell sensitivity to glucose (PG50). Proinsulin secretory ratios were increased in non‐obese T2D when compared to obese T2D. Obese T2D subjects had reduced insulin sensitivity (M/I) while non‐obese T2D subjects had insulin sensitivity that was comparable to controls.
Conclusions
In non‐obese T2D, insulin secretory defects predominate with impaired β‐cell sensitivity to glucose and proinsulin processing in the absence of insulin resistance. Future studies should consider whether different β‐cell secretory phenotypes and tissue sensitivity to insulin explain the varying responsiveness to T2D interventions.</description><identifier>ISSN: 1520-7552</identifier><identifier>EISSN: 1520-7560</identifier><identifier>DOI: 10.1002/dmrr.3295</identifier><identifier>PMID: 32017362</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Inc</publisher><subject>Arginine ; Beta cells ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Glucose ; Insulin ; Insulin resistance ; Insulin secretion ; insulin sensitivity ; Obesity ; Phenotypes ; type 2 diabetes ; β‐cell function</subject><ispartof>Diabetes/metabolism research and reviews, 2020-07, Vol.36 (5), p.e3295-n/a</ispartof><rights>2020 John Wiley & Sons Ltd</rights><rights>2020 John Wiley & Sons Ltd.</rights><rights>2020 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4435-966d29c61fcaab2c78a38a1e4b96e56af4c5250729f44cf31692648545ec85c63</citedby><cites>FETCH-LOGICAL-c4435-966d29c61fcaab2c78a38a1e4b96e56af4c5250729f44cf31692648545ec85c63</cites><orcidid>0000-0002-9253-838X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32017362$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gudipaty, Lalitha</creatorcontrib><creatorcontrib>Rosenfeld, Nora K.</creatorcontrib><creatorcontrib>Fuller, Carissa S.</creatorcontrib><creatorcontrib>Cuchel, Marina</creatorcontrib><creatorcontrib>Rickels, Michael R.</creatorcontrib><title>Different β‐cell secretory phenotype in non‐obese compared to obese early type 2 diabetes</title><title>Diabetes/metabolism research and reviews</title><addtitle>Diabetes Metab Res Rev</addtitle><description>Background
Type 2 diabetes (T2D) is characterized by impaired tissue sensitivity to insulin action (ie, insulin resistance) and impaired β‐cell insulin secretion. Because obesity contributes importantly to the development of insulin resistance, we sought to determine whether insulin secretory defects would predominate in non‐obese compared to obese T2D.
Methods
We measured β‐cell function and secretory capacity using the glucose‐potentiated arginine test in T2D subjects early in the disease course classified as non‐obese (BMI <30; n = 12) or obese (BMI ≥30 kg/m2; n = 28) and additionally compared responses from non‐obese T2D with a non‐diabetic control group (n = 12).
Results
The acute insulin response to glucose potentiation of arginine‐induced insulin release was less in non‐obese T2D than in controls and associated with impaired β‐cell sensitivity to glucose (PG50). Proinsulin secretory ratios were increased in non‐obese T2D when compared to obese T2D. Obese T2D subjects had reduced insulin sensitivity (M/I) while non‐obese T2D subjects had insulin sensitivity that was comparable to controls.
Conclusions
In non‐obese T2D, insulin secretory defects predominate with impaired β‐cell sensitivity to glucose and proinsulin processing in the absence of insulin resistance. Future studies should consider whether different β‐cell secretory phenotypes and tissue sensitivity to insulin explain the varying responsiveness to T2D interventions.</description><subject>Arginine</subject><subject>Beta cells</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Glucose</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin secretion</subject><subject>insulin sensitivity</subject><subject>Obesity</subject><subject>Phenotypes</subject><subject>type 2 diabetes</subject><subject>β‐cell function</subject><issn>1520-7552</issn><issn>1520-7560</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp1kUtKxTAUhoMovgduQAJOdHA1zavtRBDfoAiiU0OanmqlbWrSq3TmElyLC3ERrsTUqxcVHCUkHx_n_D9CaxHZjgihO3nt3DajqZhBi5GgZBQLSWand0EX0JL394QQxiWfRwuMkihmki6im4OyKMBB0-G31_fnFwNVhT0YB511PW7voLFd3wIuG9zYJhA2Aw_Y2LrVDnLcWTx5Ae2qHn-yFOelzqADv4LmCl15WP06l9H10eHV_sno7OL4dH_vbGQ4Z2KUSpnT1MioMFpn1MSJZomOgGepBCF1wY2ggsQ0LTg3BYtkSiVPBBdgEmEkW0a7E287zmrITdjH6Uq1rqy165XVpfr905R36tY-qjiRPAQUBJtfAmcfxuA7VZd-CEM3YMdeUSZIkqYsFgHd-IPe27FrwnqK8hCs4DEdhFsTyjjrvYNiOkxE1NCaGlpTQ2uBXf85_ZT8rikAOxPgqayg_9-kDs4vLz-VH-6spRc</recordid><startdate>202007</startdate><enddate>202007</enddate><creator>Gudipaty, Lalitha</creator><creator>Rosenfeld, Nora K.</creator><creator>Fuller, Carissa S.</creator><creator>Cuchel, Marina</creator><creator>Rickels, Michael R.</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9253-838X</orcidid></search><sort><creationdate>202007</creationdate><title>Different β‐cell secretory phenotype in non‐obese compared to obese early type 2 diabetes</title><author>Gudipaty, Lalitha ; Rosenfeld, Nora K. ; Fuller, Carissa S. ; Cuchel, Marina ; Rickels, Michael R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4435-966d29c61fcaab2c78a38a1e4b96e56af4c5250729f44cf31692648545ec85c63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Arginine</topic><topic>Beta cells</topic><topic>Diabetes</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Glucose</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin secretion</topic><topic>insulin sensitivity</topic><topic>Obesity</topic><topic>Phenotypes</topic><topic>type 2 diabetes</topic><topic>β‐cell function</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gudipaty, Lalitha</creatorcontrib><creatorcontrib>Rosenfeld, Nora K.</creatorcontrib><creatorcontrib>Fuller, Carissa S.</creatorcontrib><creatorcontrib>Cuchel, Marina</creatorcontrib><creatorcontrib>Rickels, Michael R.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Diabetes/metabolism research and reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gudipaty, Lalitha</au><au>Rosenfeld, Nora K.</au><au>Fuller, Carissa S.</au><au>Cuchel, Marina</au><au>Rickels, Michael R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Different β‐cell secretory phenotype in non‐obese compared to obese early type 2 diabetes</atitle><jtitle>Diabetes/metabolism research and reviews</jtitle><addtitle>Diabetes Metab Res Rev</addtitle><date>2020-07</date><risdate>2020</risdate><volume>36</volume><issue>5</issue><spage>e3295</spage><epage>n/a</epage><pages>e3295-n/a</pages><issn>1520-7552</issn><eissn>1520-7560</eissn><abstract>Background
Type 2 diabetes (T2D) is characterized by impaired tissue sensitivity to insulin action (ie, insulin resistance) and impaired β‐cell insulin secretion. Because obesity contributes importantly to the development of insulin resistance, we sought to determine whether insulin secretory defects would predominate in non‐obese compared to obese T2D.
Methods
We measured β‐cell function and secretory capacity using the glucose‐potentiated arginine test in T2D subjects early in the disease course classified as non‐obese (BMI <30; n = 12) or obese (BMI ≥30 kg/m2; n = 28) and additionally compared responses from non‐obese T2D with a non‐diabetic control group (n = 12).
Results
The acute insulin response to glucose potentiation of arginine‐induced insulin release was less in non‐obese T2D than in controls and associated with impaired β‐cell sensitivity to glucose (PG50). Proinsulin secretory ratios were increased in non‐obese T2D when compared to obese T2D. Obese T2D subjects had reduced insulin sensitivity (M/I) while non‐obese T2D subjects had insulin sensitivity that was comparable to controls.
Conclusions
In non‐obese T2D, insulin secretory defects predominate with impaired β‐cell sensitivity to glucose and proinsulin processing in the absence of insulin resistance. Future studies should consider whether different β‐cell secretory phenotypes and tissue sensitivity to insulin explain the varying responsiveness to T2D interventions.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Inc</pub><pmid>32017362</pmid><doi>10.1002/dmrr.3295</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-9253-838X</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Diabetes/metabolism research and reviews, 2020-07, Vol.36 (5), p.e3295-n/a |
| issn | 1520-7552 1520-7560 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7864552 |
| source | Wiley |
| subjects | Arginine Beta cells Diabetes Diabetes mellitus (non-insulin dependent) Glucose Insulin Insulin resistance Insulin secretion insulin sensitivity Obesity Phenotypes type 2 diabetes β‐cell function |
| title | Different β‐cell secretory phenotype in non‐obese compared to obese early type 2 diabetes |
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