Analysing uric acid levels to assess the effectiveness of dapagliflozin.

Background: Sodium-glucose cotransporter-2 inhibitors are an innovative diabetes treatment that lowers blood sugar levels without insulin. A growing body of evidence suggests that blood sugar levels are tightly correlated with uric acid levels in their blood and urine. To alleviate type 2 diabetes (T2DM) suffering, we tested dapagliflozin on serum and urinary uric acid levels of patients with T2DM and measured its efficacy in reducing uric acid levels.

FGF4 alleviates hyperglycemia in diabetes and obesity conditions.

Increasing evidence suggests that the brain plays a key role in glucose homeostasis, making it a potential target for the treatment of type 2 diabetes (T2D). Sun et al. recently reported that intracerebroventricular (ICV) administration of a single dose of fibroblast growth factor 4 (FGF4) can induce sustained T2D remission in mouse models in the absence of any risk of hypoglycemia.

Triac Treatment Prevents Neurodevelopmental and Locomotor Impairments in Thyroid Hormone Transporter Mct8/Oatp1c1 Deficient Mice.

Patients with inactive thyroid hormone (TH) transporter MCT8 display intellectual disability due to compromised central TH transport and action. As a therapeutic strategy, application of thyromimetic, MCT8-independent compounds Triac (3,5,3'-triiodothyroacetic acid), and Ditpa (3,5-diiodo-thyropropionic acid) was proposed. Here, we directly compared their thyromimetic potential in Mct8/Oatp1c1 double knock-out mice (Dko) modeling human MCT8 deficiency.

Location matters: hexokinase 1 in glucose metabolism and inflammation.

Hexokinase (HK)-1 mitochondrial-binding mechanisms and consequential physiological relevance remain unclear. Recently, De Jesus et al. studied myeloid cells with HK1 carrying mutated mitochondrial-binding domains (MBDs) and provided evidence that HK1 localization controls glucose metabolic fate.

The relevance of synuclein autoantibodies as a biomarker for Parkinson's disease.

Several studies have investigated if the levels of α-synuclein autoantibodies (α-syn AAb) differ in serum of Parkinson's disease (PD) patients and healthy subjects. Reproducible differences in their levels could serve as a biomarker for PD. The results of previous studies however remain inconclusive.

Deficiency of Thyroid Hormone Reduces Voltage-Gated Na Currents as Well as Expression of Na/K-ATPase in the Mouse Hippocampus.

Mice lacking functional thyroid follicular cells, mice, die early postnatally, making them suitable models for extreme hypothyroidism. We have previously obtained evidence in postnatal rat neurons, that a down-regulation of Na-current density could explain the reduced excitability of the nervous system in hypothyroidism. If such a mechanism underlies the development of coma and death in severe hypothyroidism, mice should show deficits in the expression of Na currents and potentially also in the expression of Na/K-ATPases, which are necessary to maintain low intracellular Na levels.

Insulin signalling in tanycytes gates hypothalamic insulin uptake and regulation of AgRP neuron activity.

Insulin acts on neurons and glial cells to regulate systemic glucose metabolism and feeding. However, the mechanisms of insulin access in discrete brain regions are incompletely defined. Here we show that insulin receptors in tanycytes, but not in brain endothelial cells, are required to regulate insulin access to the hypothalamic arcuate nucleus.

Parvocellular Oxytocin Neurons and Autism Spectrum Disorders.

The underlying mechanism of oxytocin (OT) neurons in the development of social interaction remains unclear. In a recent study, Lewis et al. characterized OT neuronal subtypes and provided evidence that expression of the autism spectrum disorder (ASD) gene Fmr1 in parvocellular OT neurons is essential for peer-peer but not filial social interactions.

NF-κB signaling in tanycytes mediates inflammation-induced anorexia.

Objectives: Infections, cancer, and systemic inflammation elicit anorexia. Despite the medical significance of this phenomenon, the question of how peripheral inflammatory mediators affect the central regulation of food intake is incompletely understood. Therefore, we have investigated the sickness behavior induced by the prototypical inflammatory mediator IL-1β.

MCH Neurons Regulate Permeability of the Median Eminence Barrier.

Melanin-concentrating hormone (MCH)-expressing neurons are key regulators of energy and glucose homeostasis. Here, we demonstrate that they provide dense projections to the median eminence (ME) in close proximity to tanycytes and fenestrated vessels. Chemogenetic activation of MCH neurons as well as optogenetic stimulation of their projections in the ME enhance permeability of the ME by increasing fenestrated vascular loops and enhance leptin action in the arcuate nucleus of the hypothalamus (ARC).

Nesfatin-1 decreases the motivational and rewarding value of food.

Homeostatic and hedonic pathways distinctly interact to control food intake. Dysregulations of circuitries controlling hedonic feeding may disrupt homeostatic mechanisms and lead to eating disorders. The anorexigenic peptides nucleobindin-2 (NUCB2)/nesfatin-1 may be involved in the interaction of these pathways.

Tissue-Specific Function of Thyroid Hormone Transporters: New Insights from Mouse Models.

Thyroid hormone (TH) transporters are required for cellular transmembrane passage of TH and are thus mandatory for proper TH metabolism and action. Consequently, inactivating mutations in TH transporters such as MCT8 or OATP1C1 can cause tissue- specific changes in TH homeostasis. As the most prominent example, patients with MCT8 mutations exhibit elevated serum T3 levels, whereas their CNS appear to be in a TH deficient state.

Differential expression patterns of sodium potassium ATPase alpha and beta subunit isoforms in mouse brain during postnatal development.

The sodium potassium ATPase (Na/K ATPase) is essential for the maintenance of a low intracellular Na and a high intracellular K concentration. Loss of function of the Na/K ATPase due to mutations in Na/K ATPase genes, anoxic conditions, depletion of ATP or inhibition of the Na/K ATPase function using cardiac glycosides such as digitalis, causes a depolarization of the resting membrane potential. While in non-excitable cells, the uptake of glucose and amino acids is decreased if the function of the Na/K ATPase is compromised, in excitable cells the symptoms range from local hyper-excitability to inactivating depolarization.

Epigallocatechin gallate (EGCG) inhibits adhesion and migration of neural progenitor cells in vitro.

Food supplements based on herbal products are widely used during pregnancy as part of a self-care approach. The idea that such supplements are safe and healthy is deeply seated in the general population, although they do not underlie the same strict safety regulations than medical drugs. We aimed to characterize the neurodevelopmental effects of the green tea catechin epigallocatechin gallate (EGCG), which is now commercialized as high-dose food supplement.