Beneficial effects of long-term liraglutide monotherapy on glycemic control and diabetic microangiopathies in a female Japanese diabetic patient with familial partial lipodystrophy 1
M. Iwanishi, C. Azuma, Y. Tezuka, Yuji Yamamoto, J. Ito-Kobayashi, M. Washiyama, A. Shimatsu, A. Mizuno, Y. Osafune
{"title":"Beneficial effects of long-term liraglutide monotherapy on glycemic control and diabetic microangiopathies in a female Japanese diabetic patient with familial partial lipodystrophy 1","authors":"M. Iwanishi, C. Azuma, Y. Tezuka, Yuji Yamamoto, J. Ito-Kobayashi, M. Washiyama, A. Shimatsu, A. Mizuno, Y. Osafune","doi":"10.15761/du.1000150","DOIUrl":null,"url":null,"abstract":"We experienced the case that a Japanese female diabetic patient with partial lipodystrophy continued liraglutide monotherapy for a long period on her will. At first examination, she had poor glycemic control and body weight reduction with decreased fat mass had been caused by uncontrolled diabetes. She had severe non-proliferative diabetic retinopathy and nephropathy with microalbuminuria. When she had weight gain after her glycemic control was improved, she still had fat loss in the lower limbs with abdominal fat excess. She had insulin deficiency and relatively severe insulin resistance. According to the clinical findings and genetic analysis, she might fit the category of familial partial lipodystrophy (FPLD)1. We administered liraglutide for her diabetes care, as previous report suggested the effectiveness of liraglutide in patients with FPLD1 for about three months. We assessed changes in fat distribution and insulin resistance during liraglutide therapy using dual energy X-ray absorptiometry (DEXA) and the oral glucose tolerance test (OGTT). Liraglutide effectively has achieved favorable glycemic and body weight control for a long period. The DEXA showed that fat mass in the upper limbs and trunk was increased, but we could speculate no further increase as her body weight was stable. The OGTT showed the amelioration of insulin resistance and insulin secretory capacity adjusted for insulin sensitivity. We thought that this might be caused by the blood-glucose-reducing effects of liraglutide and preventive effects on obesity through increasing the fat storage capacity of adipocytes. The intensified multifactorial intervention with liraglutide, anti-hypertensive drugs, and statin attenuated diabetic microangiopathies. The present case suggests that liraglutide might be as an efficient therapeutic option through its pleiotropic effects in diabetic patients with FPLD1.","PeriodicalId":309709,"journal":{"name":"Diabetes Updates","volume":"8 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Diabetes Updates","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15761/du.1000150","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
We experienced the case that a Japanese female diabetic patient with partial lipodystrophy continued liraglutide monotherapy for a long period on her will. At first examination, she had poor glycemic control and body weight reduction with decreased fat mass had been caused by uncontrolled diabetes. She had severe non-proliferative diabetic retinopathy and nephropathy with microalbuminuria. When she had weight gain after her glycemic control was improved, she still had fat loss in the lower limbs with abdominal fat excess. She had insulin deficiency and relatively severe insulin resistance. According to the clinical findings and genetic analysis, she might fit the category of familial partial lipodystrophy (FPLD)1. We administered liraglutide for her diabetes care, as previous report suggested the effectiveness of liraglutide in patients with FPLD1 for about three months. We assessed changes in fat distribution and insulin resistance during liraglutide therapy using dual energy X-ray absorptiometry (DEXA) and the oral glucose tolerance test (OGTT). Liraglutide effectively has achieved favorable glycemic and body weight control for a long period. The DEXA showed that fat mass in the upper limbs and trunk was increased, but we could speculate no further increase as her body weight was stable. The OGTT showed the amelioration of insulin resistance and insulin secretory capacity adjusted for insulin sensitivity. We thought that this might be caused by the blood-glucose-reducing effects of liraglutide and preventive effects on obesity through increasing the fat storage capacity of adipocytes. The intensified multifactorial intervention with liraglutide, anti-hypertensive drugs, and statin attenuated diabetic microangiopathies. The present case suggests that liraglutide might be as an efficient therapeutic option through its pleiotropic effects in diabetic patients with FPLD1.