Effects of insulin administration on β-cell function in subjects at high risk for type I diabetes mellitus
The aim of the study was to determine the appropriate dose of subcutaneous insulin to induce “β-cell rest” without any hypoglycemic risk, as the first step in the investigation of its potential effect in preventing or delaying clinical diabetes mellitus onset in high-risk subjects. Four subjects at...
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Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 1996-07, Vol.45 (7), p.873-875 |
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description | The aim of the study was to determine the appropriate dose of subcutaneous insulin to induce “β-cell rest” without any hypoglycemic risk, as the first step in the investigation of its potential effect in preventing or delaying clinical diabetes mellitus onset in high-risk subjects. Four subjects at high risk for type I diabetes mellitus (first-degree relatives, islet cell antibodies (ICA)-positive, and with diminished first-phase insulin secretion) were compared with four healthy individuals. After hospitalization, urinary C-peptide excretion (UCP) and 24-hour serum profiles for glucose were measured before and after administration of NPH insulin 0.1, 0.2, and 0.3 U · kg body weight per day subcutaneously in a single dose on 4 consecutive days. After insulin 0.1 U · kg body weight, a significant inhibition of endogenous insulin secretion was observed in high-risk subjects, but not in control subjects. There was no further inhibition when a higher insulin dose (0.2 and 0.3) was administered. A sustained β-cell rest was obtained after 3, 6, and 12 months of treatment with 0.1 U · kg body weight per day as outpatient therapy in high-risk subjects. With this dose, no subject developed hypoglycemia (plasma glucose |
doi_str_mv | 10.1016/S0026-0495(96)90162-6 |
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Four subjects at high risk for type I diabetes mellitus (first-degree relatives, islet cell antibodies (ICA)-positive, and with diminished first-phase insulin secretion) were compared with four healthy individuals. After hospitalization, urinary C-peptide excretion (UCP) and 24-hour serum profiles for glucose were measured before and after administration of NPH insulin 0.1, 0.2, and 0.3 U · kg body weight per day subcutaneously in a single dose on 4 consecutive days. After insulin 0.1 U · kg body weight, a significant inhibition of endogenous insulin secretion was observed in high-risk subjects, but not in control subjects. There was no further inhibition when a higher insulin dose (0.2 and 0.3) was administered. A sustained β-cell rest was obtained after 3, 6, and 12 months of treatment with 0.1 U · kg body weight per day as outpatient therapy in high-risk subjects. With this dose, no subject developed hypoglycemia (plasma glucose <50 mg/dL), whereas this adverse effect was detected after 0.2 and 0.3 U · kg body weight in both groups. In conclusion, our results indicate that administration of NPH insulin 0.1 U · kg body weight per day induces β-cell rest without the undesirable effect of hypoglycemic episodes. This is a preliminary study to investigate the potential beneficial effect of insulin in preventing or delaying type I diabetes mellitus in subjects at high risk for the disease.</description><identifier>ISSN: 0026-0495</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1016/S0026-0495(96)90162-6</identifier><identifier>PMID: 8692024</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adolescent ; Adult ; Biological and medical sciences ; Case-Control Studies ; Diabetes Mellitus, Type 1 - etiology ; Diabetes Mellitus, Type 1 - prevention & control ; diet-related diseases ; Hormones. Endocrine system ; human nutrition ; Humans ; Hypoglycemia - etiology ; Hypoglycemia - prevention & control ; Hypoglycemic Agents - administration & dosage ; Hypoglycemic Agents - adverse effects ; Injections, Subcutaneous ; Insulin - metabolism ; Insulin Secretion ; Insulin, Isophane - administration & dosage ; Insulin, Isophane - adverse effects ; Islets of Langerhans - drug effects ; Islets of Langerhans - physiology ; Medical sciences ; Middle Aged ; Pharmacology. Drug treatments ; Prediabetic State - drug therapy ; Prediabetic State - physiopathology ; Risk Factors ; Safety ; Time Factors</subject><ispartof>Metabolism, clinical and experimental, 1996-07, Vol.45 (7), p.873-875</ispartof><rights>1996</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-221c65da4d246fef96f17a8aaf8bae452edfa6eaedd337b05cd706ee1a7a76763</citedby><cites>FETCH-LOGICAL-c413t-221c65da4d246fef96f17a8aaf8bae452edfa6eaedd337b05cd706ee1a7a76763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0026-0495(96)90162-6$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3168249$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8692024$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rodríguez-Villar, C.</creatorcontrib><creatorcontrib>Conget, I.</creatorcontrib><creatorcontrib>González-Clemente, J.M.</creatorcontrib><creatorcontrib>Vidal, J.</creatorcontrib><creatorcontrib>Navarro, P.</creatorcontrib><creatorcontrib>Casamitjana, R.</creatorcontrib><creatorcontrib>Gomis, R.</creatorcontrib><title>Effects of insulin administration on β-cell function in subjects at high risk for type I diabetes mellitus</title><title>Metabolism, clinical and experimental</title><addtitle>Metabolism</addtitle><description>The aim of the study was to determine the appropriate dose of subcutaneous insulin to induce “β-cell rest” without any hypoglycemic risk, as the first step in the investigation of its potential effect in preventing or delaying clinical diabetes mellitus onset in high-risk subjects. Four subjects at high risk for type I diabetes mellitus (first-degree relatives, islet cell antibodies (ICA)-positive, and with diminished first-phase insulin secretion) were compared with four healthy individuals. After hospitalization, urinary C-peptide excretion (UCP) and 24-hour serum profiles for glucose were measured before and after administration of NPH insulin 0.1, 0.2, and 0.3 U · kg body weight per day subcutaneously in a single dose on 4 consecutive days. After insulin 0.1 U · kg body weight, a significant inhibition of endogenous insulin secretion was observed in high-risk subjects, but not in control subjects. There was no further inhibition when a higher insulin dose (0.2 and 0.3) was administered. A sustained β-cell rest was obtained after 3, 6, and 12 months of treatment with 0.1 U · kg body weight per day as outpatient therapy in high-risk subjects. With this dose, no subject developed hypoglycemia (plasma glucose <50 mg/dL), whereas this adverse effect was detected after 0.2 and 0.3 U · kg body weight in both groups. In conclusion, our results indicate that administration of NPH insulin 0.1 U · kg body weight per day induces β-cell rest without the undesirable effect of hypoglycemic episodes. This is a preliminary study to investigate the potential beneficial effect of insulin in preventing or delaying type I diabetes mellitus in subjects at high risk for the disease.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Diabetes Mellitus, Type 1 - etiology</subject><subject>Diabetes Mellitus, Type 1 - prevention & control</subject><subject>diet-related diseases</subject><subject>Hormones. Endocrine system</subject><subject>human nutrition</subject><subject>Humans</subject><subject>Hypoglycemia - etiology</subject><subject>Hypoglycemia - prevention & control</subject><subject>Hypoglycemic Agents - administration & dosage</subject><subject>Hypoglycemic Agents - adverse effects</subject><subject>Injections, Subcutaneous</subject><subject>Insulin - metabolism</subject><subject>Insulin Secretion</subject><subject>Insulin, Isophane - administration & dosage</subject><subject>Insulin, Isophane - adverse effects</subject><subject>Islets of Langerhans - drug effects</subject><subject>Islets of Langerhans - physiology</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pharmacology. Drug treatments</subject><subject>Prediabetic State - drug therapy</subject><subject>Prediabetic State - physiopathology</subject><subject>Risk Factors</subject><subject>Safety</subject><subject>Time Factors</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM9q3DAQh0VpSLfbPkKoDqW0B6eSbEv2KZSQtoFADmnOYiyNEiX-s5XkQl6rD5Jniry77DVCIJj5Rr_hI-SEs1POuPx-w5iQBava-msrv7W5JAr5hqx4XYqikYy9JasD8o68j_GBMaZUI4_JcSNbwUS1Io8XzqFJkU6O-jHOvR8p2MGPPqYAyU8jzff5f2Gw76mbR7OtZSrO3cN2EhK993f3NPj4SN0UaHraIL2k1kOHCSMd8qhPc_xAjhz0ET_u3zW5_Xnx5_x3cXX96_L8x1VhKl6mQghuZG2hsqKSDl0rHVfQALimA6xqgdaBREBry1J1rDZWMYnIQYGSSpZr8mX37yZMf2eMSQ8-LvvDiNMctWp4XZf5rEm9A02YYgzo9Cb4AcKT5kwvkvVWsl4M6lbqrWS9BJzsA-ZuQHuY2lvN_c_7PkQDvQswGh8PWMllI6o2Y592mINJw132p29vBOMl47WoqnYJOtsRmHX98xh0NB5Hg9aH7F7byb-y6guKfKSA</recordid><startdate>19960701</startdate><enddate>19960701</enddate><creator>Rodríguez-Villar, C.</creator><creator>Conget, I.</creator><creator>González-Clemente, J.M.</creator><creator>Vidal, J.</creator><creator>Navarro, P.</creator><creator>Casamitjana, R.</creator><creator>Gomis, R.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>FBQ</scope><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>19960701</creationdate><title>Effects of insulin administration on β-cell function in subjects at high risk for type I diabetes mellitus</title><author>Rodríguez-Villar, C. ; Conget, I. ; González-Clemente, J.M. ; Vidal, J. ; Navarro, P. ; Casamitjana, R. ; Gomis, R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-221c65da4d246fef96f17a8aaf8bae452edfa6eaedd337b05cd706ee1a7a76763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Diabetes Mellitus, Type 1 - etiology</topic><topic>Diabetes Mellitus, Type 1 - prevention & control</topic><topic>diet-related diseases</topic><topic>Hormones. Endocrine system</topic><topic>human nutrition</topic><topic>Humans</topic><topic>Hypoglycemia - etiology</topic><topic>Hypoglycemia - prevention & control</topic><topic>Hypoglycemic Agents - administration & dosage</topic><topic>Hypoglycemic Agents - adverse effects</topic><topic>Injections, Subcutaneous</topic><topic>Insulin - metabolism</topic><topic>Insulin Secretion</topic><topic>Insulin, Isophane - administration & dosage</topic><topic>Insulin, Isophane - adverse effects</topic><topic>Islets of Langerhans - drug effects</topic><topic>Islets of Langerhans - physiology</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pharmacology. Drug treatments</topic><topic>Prediabetic State - drug therapy</topic><topic>Prediabetic State - physiopathology</topic><topic>Risk Factors</topic><topic>Safety</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rodríguez-Villar, C.</creatorcontrib><creatorcontrib>Conget, I.</creatorcontrib><creatorcontrib>González-Clemente, J.M.</creatorcontrib><creatorcontrib>Vidal, J.</creatorcontrib><creatorcontrib>Navarro, P.</creatorcontrib><creatorcontrib>Casamitjana, R.</creatorcontrib><creatorcontrib>Gomis, R.</creatorcontrib><collection>AGRIS</collection><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>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rodríguez-Villar, C.</au><au>Conget, I.</au><au>González-Clemente, J.M.</au><au>Vidal, J.</au><au>Navarro, P.</au><au>Casamitjana, R.</au><au>Gomis, R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of insulin administration on β-cell function in subjects at high risk for type I diabetes mellitus</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>1996-07-01</date><risdate>1996</risdate><volume>45</volume><issue>7</issue><spage>873</spage><epage>875</epage><pages>873-875</pages><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract>The aim of the study was to determine the appropriate dose of subcutaneous insulin to induce “β-cell rest” without any hypoglycemic risk, as the first step in the investigation of its potential effect in preventing or delaying clinical diabetes mellitus onset in high-risk subjects. Four subjects at high risk for type I diabetes mellitus (first-degree relatives, islet cell antibodies (ICA)-positive, and with diminished first-phase insulin secretion) were compared with four healthy individuals. After hospitalization, urinary C-peptide excretion (UCP) and 24-hour serum profiles for glucose were measured before and after administration of NPH insulin 0.1, 0.2, and 0.3 U · kg body weight per day subcutaneously in a single dose on 4 consecutive days. After insulin 0.1 U · kg body weight, a significant inhibition of endogenous insulin secretion was observed in high-risk subjects, but not in control subjects. There was no further inhibition when a higher insulin dose (0.2 and 0.3) was administered. A sustained β-cell rest was obtained after 3, 6, and 12 months of treatment with 0.1 U · kg body weight per day as outpatient therapy in high-risk subjects. With this dose, no subject developed hypoglycemia (plasma glucose <50 mg/dL), whereas this adverse effect was detected after 0.2 and 0.3 U · kg body weight in both groups. In conclusion, our results indicate that administration of NPH insulin 0.1 U · kg body weight per day induces β-cell rest without the undesirable effect of hypoglycemic episodes. This is a preliminary study to investigate the potential beneficial effect of insulin in preventing or delaying type I diabetes mellitus in subjects at high risk for the disease.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8692024</pmid><doi>10.1016/S0026-0495(96)90162-6</doi><tpages>3</tpages></addata></record> |
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subjects | Adolescent Adult Biological and medical sciences Case-Control Studies Diabetes Mellitus, Type 1 - etiology Diabetes Mellitus, Type 1 - prevention & control diet-related diseases Hormones. Endocrine system human nutrition Humans Hypoglycemia - etiology Hypoglycemia - prevention & control Hypoglycemic Agents - administration & dosage Hypoglycemic Agents - adverse effects Injections, Subcutaneous Insulin - metabolism Insulin Secretion Insulin, Isophane - administration & dosage Insulin, Isophane - adverse effects Islets of Langerhans - drug effects Islets of Langerhans - physiology Medical sciences Middle Aged Pharmacology. Drug treatments Prediabetic State - drug therapy Prediabetic State - physiopathology Risk Factors Safety Time Factors |
title | Effects of insulin administration on β-cell function in subjects at high risk for type I diabetes mellitus |
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