{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:22:31Z","timestamp":1791332551695,"version":"4.3.1"},"reference-count":31,"publisher":"American Diabetes Association","issue":"4","license":[{"start":{"date-parts":[[2021,8,28]],"date-time":"2021-08-28T00:00:00Z","timestamp":1630108800000},"content-version":"vor","delay-in-days":2730,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/3.0\/"}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,4,1]]},"abstract":"<jats:sec>\n                  <jats:title>OBJECTIVE<\/jats:title>\n                  <jats:p>Leptin administration is known to directly modulate pancreatic \u03b2-cell function in leptin-deficient rodent models. However, human studies examining the effects of leptin administration on \u03b2-cell function are lacking. In this study, we examined the effects (16\u201320 weeks) of leptin replacement on \u03b2-cell function in patients with lipodystrophy.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                  <jats:p>In a prospective, open-label, currently ongoing study, we studied the effects of leptin replacement on \u03b2-cell function in 13 patients with congenital or acquired lipodystrophy. Insulin secretory rate (ISR) was calculated by C-peptide deconvolution from plasma glucose and C-peptide levels measured during oral glucose tolerance tests (OGTTs) performed at baseline and after 16\u201320 weeks of leptin replacement. \u03b2-Cell glucose sensitivity and rate sensitivity were assessed by mathematical modeling of OGTT.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>There was a significant decrease in triglycerides, free fatty acids, and glycosylated hemoglobin levels (A1C) after leptin therapy. Patients with lipodystrophy have high fasting and glucose-stimulated ISR. However, leptin therapy had no significant effect on fasting ISR, total insulin secretion during OGTT, \u03b2-cell glucose sensitivity, rate sensitivity, or insulin clearance.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>In contrast to the suppressive effects of leptin on \u03b2-cell function in rodents, 16\u201320-week treatment with leptin in lipodystrophy patients did not significantly affect insulin secretion or \u03b2-cell function in leptin-deficient individuals with lipodystrophy.<\/jats:p>\n               <\/jats:sec>","DOI":"10.2337\/dc13-2040","type":"journal-article","created":{"date-parts":[[2014,2,5]],"date-time":"2014-02-05T04:36:01Z","timestamp":1391574961000},"page":"1101-1107","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":22,"title":["Effects of Leptin Replacement Therapy on Pancreatic \u03b2-Cell Function in Patients With Lipodystrophy"],"prefix":"10.2337","volume":"37","author":[{"given":"Ranganath","family":"Muniyappa","sequence":"first","affiliation":[{"name":"Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca J.","family":"Brown","sequence":"additional","affiliation":[{"name":"Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea","family":"Mari","sequence":"additional","affiliation":[{"name":"Institute of Biomedical Engineering, National Research Council, Padova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jalaja","family":"Joseph","sequence":"additional","affiliation":[{"name":"Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary A.","family":"Warren","sequence":"additional","affiliation":[{"name":"Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elaine K.","family":"Cochran","sequence":"additional","affiliation":[{"name":"Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monica C.","family":"Skarulis","sequence":"additional","affiliation":[{"name":"Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of 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