Therefore, insulin resistance and alterations in liver structure, most likely early stages of non-alcoholic fatty liver disease, seem to be relevant in type 1 diabetes and do not only lead to elevated plasma levels of asprosin, but also to a blunted asprosin response in hypoglycemia.
In addition, a rapid elevation of HSL levels was detected after insulin injection in patients, which suggests that the inhibitory effects of insulin on HSL can be overridden by insulin-induced hypoglycemia.
Bolus insulin administration to fasted mice resulted in hypoglycemia, which increased hypothalamo-pituitary-adrenal (HPA) axis- and sympathetic activity, increased transcription of neuropeptide Y (Npy) and agouti-related peptide (Agrp) in the hypothalamic arcuate nucleus and activated IBA1+ microglia in the hypothalamus.
Thus altered expression of Neuregulin 1, ErbB receptor subtypes and Ki67 during diabetes and hypoglycemia contributes to reduced cellular proliferation and deficits in motor function.
Respondents with or without the condition of interest (CVD-related comorbidities or hypoglycaemia) were compared via generalized linear models in terms of the outcome variables: (1) health-related quality of life (HRQoL), (2) work productivity and activity impairment, (3) healthcare resource utilization and (4) economic costs.
Synergistic anti-neoplastic effects of the metformin/hypoglycemia combination were mediated by glycogen synthase kinase 3β (GSK3β) activation downstream of PP2A, leading to a decline in the pro-survival protein MCL-1, and cell death.
We recorded DM or CVD-related emergency visit or hospitalisation, change in BMI, systolic and diastolic BP, lipids profile, e-GFR, HBA1c, and frequency of hypoglycemia during Ramadan fasting and not -fasting period.
DU145 and PC3 CRPC cell lines were exposed to 20 μM imatinib under 5 mM (hypoglycemia) or 30 mM glucose (hyperglycemia) for 48-72 h. Cell viability was assessed by the MTS assay.
NO neurons exhibited ERα/β-dependent (beta<sub>1</sub> AR, GPER) and -independent (alpha<sub>1</sub> AR) sex differences in receptor protein responses to hypoglycemia.
The energy gauge AMPK is activated in DVC metabolic-sensory A2 noradrenergic neurons by hypoglycemia-associated lactoprivation, but sensor reactivity is diminished by antecedent hypoglycemia (AH).
We studied the consequences of elevated levels of Pfkfb3, a key regulatory enzyme of glycolysis, and found that pharmacological inhibition of Pfkfb3 with the small molecule 3PO reversed hypoglycemia and reduced hematopoietic manifestations of MPNs.
In this study, we tested whether stimulation of GPR119, a G-protein-coupled receptor expressed in pancreatic islet as well as enteroendocrine cells and previously shown to stimulate insulin and incretin secretion, might enhance glucagon secretion during hypoglycemia.
Participants started insulin glargine and completed QoL-questionnaires (WHO-5 Well-being Index (WHO-5; emotional well-being), Hypoglycaemia Fear Survey-worry scale (HFS-w; hypoglycaemia fear) and Diabetes Symptom Checklist-revised (DSC-r; diabetes symptom distress) at baseline, 3 and 6 months follow-up.
In this study, we tested whether stimulation of GPR119, a G-protein-coupled receptor expressed in pancreatic islet as well as enteroendocrine cells and previously shown to stimulate insulin and incretin secretion, might enhance glucagon secretion during hypoglycemia.
In this study, we tested whether stimulation of GPR119, a G-protein-coupled receptor expressed in pancreatic islet as well as enteroendocrine cells and previously shown to stimulate insulin and incretin secretion, might enhance glucagon secretion during hypoglycemia.
We explored the risks associated with metformin plus sulfonylurea (MET + SU) or MET plus a dipeptidyl peptidase-4 inhibitor (MET + DPP4i) for hypoglycemia, cardiovascular disease (CVD) events and all-cause mortality in type 2 diabetes (T2D) patients with comorbidities.
In this study, we tested whether stimulation of GPR119, a G-protein-coupled receptor expressed in pancreatic islet as well as enteroendocrine cells and previously shown to stimulate insulin and incretin secretion, might enhance glucagon secretion during hypoglycemia.
In response to insulin-induced hypoglycemia, endogenous glucose production did not change from before to 6 months (0.42 ± 0.08 vs 0.54 ± 0.07 mg·kg-1·min-1) but improved after 18 months (0.84 ± 0.15 mg·kg-1·min-1; P < 0.05 vs before CGM), albeit remaining less than in controls (1.39 ± 0.11 mg·kg-1·min-1; P ≤ 0.01 vs all).