Restoration of Lepr in β cells of Lepr null mice does not prevent hyperinsulinemia and hyperglycemia
نویسندگان
چکیده
منابع مشابه
Restoration of Lepr in β cells of Lepr null mice does not prevent hyperinsulinemia and hyperglycemia
OBJECTIVE The adipose-derived hormone leptin plays an important role in regulating body weight and glucose homeostasis. Leptin receptors are expressed in the central nervous system as well as peripheral tissues involved in regulating glucose homeostasis, including insulin-producing β cells of the pancreas. Previous studies assessing the role of leptin receptors in β cells used Cre-loxP to disru...
متن کاملHyperglycemia in rodent models of type 2 diabetes requires insulin-resistant alpha cells.
To determine the role of glucagon action in diet-induced and genetic type 2 diabetes (T2D), we studied high-fat-diet-induced obese (DIO) and leptin receptor-defective (LepR(-/-)) rodents with and without glucagon receptors (GcgRs). DIO and LepR(-/-),GcgR(+/+) mice both developed hyperinsulinemia, increased liver sterol response element binding protein 1c, and obesity. DIO GcgR(+/+) mice develop...
متن کاملDefects in Innate Immunity Predispose C57BL/6J-Lepr/Lepr Mice to Infection by Staphylococcus aureus
Foot and ankle infections are the most common cause of hospitalization among diabetic patients, and Staphylococcus aureus is a major pathogen implicated in these infections. Patients with insulin-resistant (type 2) diabetes are more susceptible to bacterial infections than nondiabetic subjects, but the pathogenesis of these infections is poorly understood. C57BL/6J-Lepr/Lepr (hereafter, db/db) ...
متن کاملTransgenic complementation of leptin-receptor deficiency. I. Rescue of the obesity/diabetes phenotype of LEPR-null mice expressing a LEPR-B transgene.
Mice homozygous for the Leprdb3J (db3J) mutation are null for all known isoforms of the leptin receptor (LEPR). These animals are obese, hyperphagic, cold intolerant, insulin resistant, and infertile. Mice homozygous for the Leprdb (db) mutation (lacking the B isoform only) have the same phenotype as db3J animals. To better understand the function(s) of the LEPR isoforms in vivo, we generated d...
متن کاملHyperinsulinemia does not change atherosclerosis development in apolipoprotein E null mice.
OBJECTIVE To determine the contribution of hyperinsulinemia to atherosclerosis development. METHODS AND RESULTS Apolipoprotein E (Apoe) null mice that had knockout of a single allele of the insulin receptor (Insr) gene were compared with littermate Apoe null mice with intact insulin receptors. Plasma insulin levels in Insr haploinsufficient/Apoe null mice were 50% higher in the fasting state ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Molecular Metabolism
سال: 2017
ISSN: 2212-8778
DOI: 10.1016/j.molmet.2017.04.003