Insulin receptors (IRs) and insulin signaling proteins are widely distributed throughout the central nervous system (CNS). To study the physiological role of insulin signaling in the brain, we created mice with a neuron-specific disruption of the IR gene (NIRKO mice). Inactivation of the IR had no impact on brain development or neuronal survival. However, female NIRKO mice showed increased food intake, and both male and female mice developed diet-sensitive obesity with increases in body fat and plasma leptin levels, mild insulin resistance, elevated plasma insulin levels, and hypertriglyceridemia. NIRKO mice also exhibited impaired spermatogenesis and ovarian follicle maturation because of hypothalamic dysregulation of luteinizing hormone. Thus, IR signaling in the CNS plays an important role in regulation of energy disposal, fuel metabolism, and reproduction.

Background Since December 2019 the novel coronavirus disease 2019 (COVID-19) has been burdening all health systems worldwide. However, pulmonary and extrapulmonary sequelae of COVID-19 after recovery from the acute disease are unknown. Material and methods Hospitalized COVID-19 patients not requiring mechanical ventilation were included and followed 6 weeks after discharge. Body plethysmography, lung diffusion capacity (DLco), blood gas analysis (ABG), 6-min walk test (6MWT), echocardiography, and laboratory tests were performed. Quality of life (QoL), depression, and anxiety were assessed using validated questionnaires. Results 33 patients with severe disease were included. Patients were discharged without prophylactic anticoagulation. At follow-up there were no thromboembolic complications in any patient. 11 patients (33%) had dyspnea, 11 (33%) had cough, and 15 (45%) suffered from symptoms of fatigue. Pulmonary function tests including ABG did not reveal any limitations (TLC: median = 94% of predicted [IQR:85–105]; VC: 93% [78–101]; FEV1: 95% [72–103]; FEV1/FVC 79% [76–85]; PaO2: 72 mmHg [67–79]; PaCO2: 38 mmHg (Xu et al., 2020; Tian et al., 2020; Huang et al., 2020; Ware, 2013) [35-38], except for slightly reduced DLco (77% [69–95]). There were no echocardiographic impairments. 6MWT distance was reduced in most patients without oxygen desaturation. According to standardized questionnaires, patients suffered from reduced QoL, mainly due to decreased mobility (SGRQ activity score: 54 [19–78]). There were no indicators for depression or anxiety (PHQ-9: 7 [4] , [5] , [6] , [7] , [8] , [9] , [10] , [11] ( Mizumoto et al., 2020; Kimball et al., 2020; Sakurai et al., 2020; Tabata et al., 2020; Wu and McGoogan, 2020; Richardson et al., 2020; Lewnard et al., 2020; Wang et al., 2020) [4] , [5] , [6] , [7] , [8] , [9] , [10] , [11] 4-11, GAD-7: 4 [1] , [2] , [3] , [4] , [5] , [6] , [7] , [8] , [9] ( Lu et al., 2020; Zhou et al., 2020; Zhu et al., 2020; Mizumoto et al., 2020; Kimball et al., 2020; Sakurai et al., 2020; Tabata et al., 2020; Wu and McGoogan, 2020; Richardson et al., 2020) [1] , [2] , [3] , [4] , [5] , [6] , ...

A Pro115Gln mutation in PPARgamma2 accelerates the differentiation of adipocytes and may cause obesity.

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Definition of Diabetes MellitusDiabetes mellitus is the collective term for heterogeneous metabolic disorders whose main finding is chronic hyperglycaemia. The cause is either a disturbed insulin secretion or a disturbed insulin effect or usually both. Gestational DiabetesGlucose tolerance disorder that occurs or is diagnosed for the first time during pregnancy [1].Type 1 diabetes ▪ β-cell destruction that leads to an absolute insulin, deficiency mostly transmitted immunologically, ▪ Checkpoint inhibitor-induced diabetes, ▪ LADA (latent autoimmune diabetes in adults): classified as type 1 diabetes ( ▶ Table 1).Type 2 diabetes ▪ Can range from a predominant insulin resistance with a relative insulin deficiency to a largely secretory defect with insulin resistance. ▪ Is often associated with other diseases (e. g. the metabolic syndrome).Other specific types of diabetes ▪ Exocrine pancreatic diseases (e. g. pancreatitis, cystic fibrosis, hemochromatosis), ▪ Endocrinopathies (e. g. Cushing's syndrome, acromegaly, pheochromocytoma), ▪ Medically-chemically induced (e. g. glucocorticoids, neuroleptics, interferon-alpha, pentamidine).Genetic defects of the β-cell function (e. g. MODY forms)▪ Genetic defects of insulin action, S1 S1This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited.