One-year metreleptin improves insulin secretion in patients with diabetes linked to genetic lipodystrophic syndromes
Recombinant methionyl human leptin (metreleptin) therapy was shown to improve hyperglycaemia, dyslipidaemia and insulin sensitivity in patients with lipodystrophic syndromes, but its effects on insulin secretion remain controversial. We used dynamic intravenous (i.v.) clamp procedures to measure ins...
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| Veröffentlicht in: | Diabetes, obesity & metabolism obesity & metabolism, 2016-07, Vol.18 (7), p.693-697 |
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| creator | Vatier, C. Fetita, S. Boudou, P. Tchankou, C. Deville, L. Riveline, JP Young, J. Mathivon, L. Travert, F. Morin, D. Cahen, J. Lascols, O. Andreelli, F. Reznik, Y. Mongeois, E. Madelaine, I. Vantyghem, MC Gautier, JF Vigouroux, C. |
| description | Recombinant methionyl human leptin (metreleptin) therapy was shown to improve hyperglycaemia, dyslipidaemia and insulin sensitivity in patients with lipodystrophic syndromes, but its effects on insulin secretion remain controversial. We used dynamic intravenous (i.v.) clamp procedures to measure insulin secretion, adjusted to insulin sensitivity, at baseline and after 1 year of metreleptin therapy, in 16 consecutive patients with lipodystrophy, diabetes and leptin deficiency. Patients, with a mean [± standard error of the mean (s.e.m.)] age of 39.2 (±4) years, presented with familial partial lipodystrophy (n = 11, 10 women) or congenital generalized lipodystrophy (n = 5, four women). Their mean (± s.e.m.) BMI (23.9 ± 0.7 kg/m2), glycated haemoglobin levels (8.5 ± 0.4%) and serum triglycerides levels (4.6 ± 0.9 mmol/l) significantly decreased within 1 month of metreleptin therapy, then remained stable. Insulin sensitivity (from hyperglycaemic or euglycaemic‐hyperinsulinaemic clamps, n = 4 and n = 12, respectively), insulin secretion during graded glucose infusion (n = 12), and acute insulin response to i.v. glucose adjusted to insulin sensitivity (disposition index, n = 12), significantly increased after 1 year of metreleptin therapy. The increase in disposition index was related to a decrease in percentage of total and trunk body fat. Metreleptin therapy improves not only insulin sensitivity, but also insulin secretion in patients with diabetes attributable to genetic lipodystrophies. |
| doi_str_mv | 10.1111/dom.12606 |
| format | Article |
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We used dynamic intravenous (i.v.) clamp procedures to measure insulin secretion, adjusted to insulin sensitivity, at baseline and after 1 year of metreleptin therapy, in 16 consecutive patients with lipodystrophy, diabetes and leptin deficiency. Patients, with a mean [± standard error of the mean (s.e.m.)] age of 39.2 (±4) years, presented with familial partial lipodystrophy (n = 11, 10 women) or congenital generalized lipodystrophy (n = 5, four women). Their mean (± s.e.m.) BMI (23.9 ± 0.7 kg/m2), glycated haemoglobin levels (8.5 ± 0.4%) and serum triglycerides levels (4.6 ± 0.9 mmol/l) significantly decreased within 1 month of metreleptin therapy, then remained stable. Insulin sensitivity (from hyperglycaemic or euglycaemic‐hyperinsulinaemic clamps, n = 4 and n = 12, respectively), insulin secretion during graded glucose infusion (n = 12), and acute insulin response to i.v. glucose adjusted to insulin sensitivity (disposition index, n = 12), significantly increased after 1 year of metreleptin therapy. The increase in disposition index was related to a decrease in percentage of total and trunk body fat. Metreleptin therapy improves not only insulin sensitivity, but also insulin secretion in patients with diabetes attributable to genetic lipodystrophies.</description><identifier>ISSN: 1462-8902</identifier><identifier>EISSN: 1463-1326</identifier><identifier>DOI: 10.1111/dom.12606</identifier><identifier>PMID: 26584826</identifier><identifier>CODEN: DOMEF6</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Body fat ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 1 - drug therapy ; Diabetes Mellitus, Type 1 - metabolism ; Dyslipidemia ; Endocrinology and metabolism ; Female ; glucose metabolism ; Glycated Hemoglobin A - metabolism ; Hemoglobin ; Human health and pathology ; Humans ; Hyperglycemia ; Hyperglycemia - chemically induced ; Hypoglycemic Agents - therapeutic use ; Hypolipidemic Agents - therapeutic use ; Insulin ; Insulin - administration & dosage ; Insulin - metabolism ; insulin resistance ; Insulin Resistance - physiology ; Insulin Secretion ; Lamin Type A - genetics ; Leptin ; Leptin - analogs & derivatives ; Leptin - deficiency ; Leptin - therapeutic use ; Life Sciences ; Lipodystrophy ; Lipodystrophy - drug therapy ; Lipodystrophy - genetics ; Male ; Mutation - genetics ; observational study ; Santé publique et épidémiologie ; Secretion ; Syndrome ; Triglycerides ; Triglycerides - metabolism</subject><ispartof>Diabetes, obesity & metabolism, 2016-07, Vol.18 (7), p.693-697</ispartof><rights>2015 John Wiley & Sons Ltd</rights><rights>2015 John Wiley & Sons Ltd.</rights><rights>2016 John Wiley & Sons Ltd</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4886-c01bc34451841e22c8f6bebbc3ea02b5b12461eb12d7e8fae9e7078bf6be994c3</citedby><cites>FETCH-LOGICAL-c4886-c01bc34451841e22c8f6bebbc3ea02b5b12461eb12d7e8fae9e7078bf6be994c3</cites><orcidid>0000-0002-8181-4721</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fdom.12606$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fdom.12606$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26584826$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.sorbonne-universite.fr/hal-01259859$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Vatier, C.</creatorcontrib><creatorcontrib>Fetita, S.</creatorcontrib><creatorcontrib>Boudou, P.</creatorcontrib><creatorcontrib>Tchankou, C.</creatorcontrib><creatorcontrib>Deville, L.</creatorcontrib><creatorcontrib>Riveline, JP</creatorcontrib><creatorcontrib>Young, J.</creatorcontrib><creatorcontrib>Mathivon, L.</creatorcontrib><creatorcontrib>Travert, F.</creatorcontrib><creatorcontrib>Morin, D.</creatorcontrib><creatorcontrib>Cahen, J.</creatorcontrib><creatorcontrib>Lascols, O.</creatorcontrib><creatorcontrib>Andreelli, F.</creatorcontrib><creatorcontrib>Reznik, Y.</creatorcontrib><creatorcontrib>Mongeois, E.</creatorcontrib><creatorcontrib>Madelaine, I.</creatorcontrib><creatorcontrib>Vantyghem, MC</creatorcontrib><creatorcontrib>Gautier, JF</creatorcontrib><creatorcontrib>Vigouroux, C.</creatorcontrib><title>One-year metreleptin improves insulin secretion in patients with diabetes linked to genetic lipodystrophic syndromes</title><title>Diabetes, obesity & metabolism</title><addtitle>Diabetes Obes Metab</addtitle><description>Recombinant methionyl human leptin (metreleptin) therapy was shown to improve hyperglycaemia, dyslipidaemia and insulin sensitivity in patients with lipodystrophic syndromes, but its effects on insulin secretion remain controversial. We used dynamic intravenous (i.v.) clamp procedures to measure insulin secretion, adjusted to insulin sensitivity, at baseline and after 1 year of metreleptin therapy, in 16 consecutive patients with lipodystrophy, diabetes and leptin deficiency. Patients, with a mean [± standard error of the mean (s.e.m.)] age of 39.2 (±4) years, presented with familial partial lipodystrophy (n = 11, 10 women) or congenital generalized lipodystrophy (n = 5, four women). Their mean (± s.e.m.) BMI (23.9 ± 0.7 kg/m2), glycated haemoglobin levels (8.5 ± 0.4%) and serum triglycerides levels (4.6 ± 0.9 mmol/l) significantly decreased within 1 month of metreleptin therapy, then remained stable. Insulin sensitivity (from hyperglycaemic or euglycaemic‐hyperinsulinaemic clamps, n = 4 and n = 12, respectively), insulin secretion during graded glucose infusion (n = 12), and acute insulin response to i.v. glucose adjusted to insulin sensitivity (disposition index, n = 12), significantly increased after 1 year of metreleptin therapy. The increase in disposition index was related to a decrease in percentage of total and trunk body fat. Metreleptin therapy improves not only insulin sensitivity, but also insulin secretion in patients with diabetes attributable to genetic lipodystrophies.</description><subject>Adult</subject><subject>Body fat</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 1 - drug therapy</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Dyslipidemia</subject><subject>Endocrinology and metabolism</subject><subject>Female</subject><subject>glucose metabolism</subject><subject>Glycated Hemoglobin A - metabolism</subject><subject>Hemoglobin</subject><subject>Human health and pathology</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Hyperglycemia - chemically induced</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Hypolipidemic Agents - therapeutic use</subject><subject>Insulin</subject><subject>Insulin - administration & dosage</subject><subject>Insulin - metabolism</subject><subject>insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>Insulin Secretion</subject><subject>Lamin Type A - genetics</subject><subject>Leptin</subject><subject>Leptin - analogs & derivatives</subject><subject>Leptin - deficiency</subject><subject>Leptin - therapeutic use</subject><subject>Life Sciences</subject><subject>Lipodystrophy</subject><subject>Lipodystrophy - drug therapy</subject><subject>Lipodystrophy - genetics</subject><subject>Male</subject><subject>Mutation - genetics</subject><subject>observational study</subject><subject>Santé publique et épidémiologie</subject><subject>Secretion</subject><subject>Syndrome</subject><subject>Triglycerides</subject><subject>Triglycerides - metabolism</subject><issn>1462-8902</issn><issn>1463-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU9v1DAQxSMEoqVw4AugSFzgkNb_4jjHUugWaWFBKnC0nGSWdZvYwXZa8u2Z7bZ7QAJfxn7-zdOMXpa9pOSY4jnp_HBMmSTyUXZIheQF5Uw-vruzQtWEHWTPYrwihAiuqqfZAZOlEorJwyytHBQzmJAPkAL0MCbrcjuMwd9AzK2LU49ChDZAsh6_XD6aZMGlmN_atMk7axpIyCJ3DV2efP4THMItKqPv5piCHzf4jLPrgh8gPs-erE0f4cV9Pcq-nX-4PLsolqvFx7PTZdEKpWTREtq0XIiSKkGBsVatZQMNamAIa8qGMiEpYOkqUGsDNVSkUs2WqmvR8qPs7c53Y3o9BjuYMGtvrL44XeqtRigra1XWNxTZNzsWN_81QUx6sLGFvjcO_BQ1rWopFWclQ_T1X-iVn4LDTTQnZS1wBir_R6FXqTgX6LcfsQ0-xgDr_ZyU6G24GsPVd-Ei--recWoG6PbkQ5oInOyAW9vD_G8n_X716cGy2HXYmOD3vsOEay0rXpX6x-eFvvy-OP_6brnQX_gfRx6-Dw</recordid><startdate>201607</startdate><enddate>201607</enddate><creator>Vatier, C.</creator><creator>Fetita, S.</creator><creator>Boudou, P.</creator><creator>Tchankou, C.</creator><creator>Deville, L.</creator><creator>Riveline, JP</creator><creator>Young, J.</creator><creator>Mathivon, L.</creator><creator>Travert, F.</creator><creator>Morin, D.</creator><creator>Cahen, J.</creator><creator>Lascols, O.</creator><creator>Andreelli, F.</creator><creator>Reznik, Y.</creator><creator>Mongeois, E.</creator><creator>Madelaine, I.</creator><creator>Vantyghem, MC</creator><creator>Gautier, JF</creator><creator>Vigouroux, C.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><general>Wiley</general><scope>BSCLL</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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><orcidid>https://orcid.org/0000-0002-8181-4721</orcidid></search><sort><creationdate>201607</creationdate><title>One-year metreleptin improves insulin secretion in patients with diabetes linked to genetic lipodystrophic syndromes</title><author>Vatier, C. ; Fetita, S. ; Boudou, P. ; Tchankou, C. ; Deville, L. ; Riveline, JP ; Young, J. ; Mathivon, L. ; Travert, F. ; Morin, D. ; Cahen, J. ; Lascols, O. ; Andreelli, F. ; Reznik, Y. ; Mongeois, E. ; Madelaine, I. ; Vantyghem, MC ; Gautier, JF ; Vigouroux, C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4886-c01bc34451841e22c8f6bebbc3ea02b5b12461eb12d7e8fae9e7078bf6be994c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Body fat</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 1 - drug therapy</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Dyslipidemia</topic><topic>Endocrinology and metabolism</topic><topic>Female</topic><topic>glucose metabolism</topic><topic>Glycated Hemoglobin A - metabolism</topic><topic>Hemoglobin</topic><topic>Human health and pathology</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Hyperglycemia - chemically induced</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Hypolipidemic Agents - therapeutic use</topic><topic>Insulin</topic><topic>Insulin - administration & dosage</topic><topic>Insulin - metabolism</topic><topic>insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>Insulin Secretion</topic><topic>Lamin Type A - genetics</topic><topic>Leptin</topic><topic>Leptin - analogs & derivatives</topic><topic>Leptin - deficiency</topic><topic>Leptin - therapeutic use</topic><topic>Life Sciences</topic><topic>Lipodystrophy</topic><topic>Lipodystrophy - drug therapy</topic><topic>Lipodystrophy - genetics</topic><topic>Male</topic><topic>Mutation - genetics</topic><topic>observational study</topic><topic>Santé publique et épidémiologie</topic><topic>Secretion</topic><topic>Syndrome</topic><topic>Triglycerides</topic><topic>Triglycerides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vatier, C.</creatorcontrib><creatorcontrib>Fetita, S.</creatorcontrib><creatorcontrib>Boudou, P.</creatorcontrib><creatorcontrib>Tchankou, C.</creatorcontrib><creatorcontrib>Deville, L.</creatorcontrib><creatorcontrib>Riveline, JP</creatorcontrib><creatorcontrib>Young, J.</creatorcontrib><creatorcontrib>Mathivon, L.</creatorcontrib><creatorcontrib>Travert, F.</creatorcontrib><creatorcontrib>Morin, D.</creatorcontrib><creatorcontrib>Cahen, J.</creatorcontrib><creatorcontrib>Lascols, O.</creatorcontrib><creatorcontrib>Andreelli, F.</creatorcontrib><creatorcontrib>Reznik, Y.</creatorcontrib><creatorcontrib>Mongeois, E.</creatorcontrib><creatorcontrib>Madelaine, I.</creatorcontrib><creatorcontrib>Vantyghem, MC</creatorcontrib><creatorcontrib>Gautier, JF</creatorcontrib><creatorcontrib>Vigouroux, C.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><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>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>Diabetes, obesity & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vatier, C.</au><au>Fetita, S.</au><au>Boudou, P.</au><au>Tchankou, C.</au><au>Deville, L.</au><au>Riveline, JP</au><au>Young, J.</au><au>Mathivon, L.</au><au>Travert, F.</au><au>Morin, D.</au><au>Cahen, J.</au><au>Lascols, O.</au><au>Andreelli, F.</au><au>Reznik, Y.</au><au>Mongeois, E.</au><au>Madelaine, I.</au><au>Vantyghem, MC</au><au>Gautier, JF</au><au>Vigouroux, C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>One-year metreleptin improves insulin secretion in patients with diabetes linked to genetic lipodystrophic syndromes</atitle><jtitle>Diabetes, obesity & metabolism</jtitle><addtitle>Diabetes Obes Metab</addtitle><date>2016-07</date><risdate>2016</risdate><volume>18</volume><issue>7</issue><spage>693</spage><epage>697</epage><pages>693-697</pages><issn>1462-8902</issn><eissn>1463-1326</eissn><coden>DOMEF6</coden><abstract>Recombinant methionyl human leptin (metreleptin) therapy was shown to improve hyperglycaemia, dyslipidaemia and insulin sensitivity in patients with lipodystrophic syndromes, but its effects on insulin secretion remain controversial. We used dynamic intravenous (i.v.) clamp procedures to measure insulin secretion, adjusted to insulin sensitivity, at baseline and after 1 year of metreleptin therapy, in 16 consecutive patients with lipodystrophy, diabetes and leptin deficiency. Patients, with a mean [± standard error of the mean (s.e.m.)] age of 39.2 (±4) years, presented with familial partial lipodystrophy (n = 11, 10 women) or congenital generalized lipodystrophy (n = 5, four women). Their mean (± s.e.m.) BMI (23.9 ± 0.7 kg/m2), glycated haemoglobin levels (8.5 ± 0.4%) and serum triglycerides levels (4.6 ± 0.9 mmol/l) significantly decreased within 1 month of metreleptin therapy, then remained stable. Insulin sensitivity (from hyperglycaemic or euglycaemic‐hyperinsulinaemic clamps, n = 4 and n = 12, respectively), insulin secretion during graded glucose infusion (n = 12), and acute insulin response to i.v. glucose adjusted to insulin sensitivity (disposition index, n = 12), significantly increased after 1 year of metreleptin therapy. The increase in disposition index was related to a decrease in percentage of total and trunk body fat. Metreleptin therapy improves not only insulin sensitivity, but also insulin secretion in patients with diabetes attributable to genetic lipodystrophies.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>26584826</pmid><doi>10.1111/dom.12606</doi><tpages>5</tpages><orcidid>https://orcid.org/0000-0002-8181-4721</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Diabetes, obesity & metabolism, 2016-07, Vol.18 (7), p.693-697 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Adult Body fat Diabetes Diabetes mellitus Diabetes Mellitus, Type 1 - drug therapy Diabetes Mellitus, Type 1 - metabolism Dyslipidemia Endocrinology and metabolism Female glucose metabolism Glycated Hemoglobin A - metabolism Hemoglobin Human health and pathology Humans Hyperglycemia Hyperglycemia - chemically induced Hypoglycemic Agents - therapeutic use Hypolipidemic Agents - therapeutic use Insulin Insulin - administration & dosage Insulin - metabolism insulin resistance Insulin Resistance - physiology Insulin Secretion Lamin Type A - genetics Leptin Leptin - analogs & derivatives Leptin - deficiency Leptin - therapeutic use Life Sciences Lipodystrophy Lipodystrophy - drug therapy Lipodystrophy - genetics Male Mutation - genetics observational study Santé publique et épidémiologie Secretion Syndrome Triglycerides Triglycerides - metabolism |
| title | One-year metreleptin improves insulin secretion in patients with diabetes linked to genetic lipodystrophic syndromes |
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