High glucose induces tau hyperphosphorylation in hippocampal neurons via inhibition of ALKBH5-mediated Dgkh mA demethylation: a potential mechanism for diabetic cognitive dysfunction.

Tau hyperphosphorylation in hippocampal neurons has an important pathogenetic role in the development of diabetic cognitive dysfunction. N-methyladenosine (mA) methylation is the most common modification of eukaryotic mRNA and is involved in regulating diverse biological processes. However, the role of mA alteration in tau hyperphosphorylation of hippocampus neurons has not been reported.

Changed cerebral function and morphology serve as neuroimaging evidence for subclinical type 2 diabetic polyneuropathy.

Introduction: Central and peripheral nervous systems are all involved in type 2 diabetic polyneuropathy mechanisms, but such subclinical changes and associations remain unknown. This study aims to explore subclinical changes of the central and peripheral and unveil their association.

Methods: A total of 55 type-2 diabetes patients consisting of symptomatic (n = 23), subclinical (n = 12), and no polyneuropathy (n = 20) were enrolled in this study.

Favorable Genotypes of Type III Interferon Confer Risk of Dyslipidemia in the Population With Obesity.

Background: Studies have indicated that the chronic state of inflammation caused by obesity leads to dyslipidemia. However, how the polymorphisms involved in these inflammatory pathways affect the lipid metabolism in people with obesity is poorly understood. We investigated the associations of inflammation-related gene polymorphisms with dyslipidemia in individuals with obesity living in China.

Associations of TCF7L2 rs11196218 (A/G) and GLP-1R rs761386 (C/T) Gene Polymorphisms with Obesity in Chinese Population.

Introduction: This study aimed to investigate the genetic polymorphism associations with obesity of the transcription factor 7-like 2 () gene rs11196218 (A/G) and glucagon-like peptide 1 receptor () gene rs761386 (C/T) in the Chinese population.

Patients And Methods: This was a case-control pilot study involving 60 patients with obesity and 69 non-obesity Chinese adults, and the two groups were sex and age matched. Anthropometric indices of obesity, fasting blood glucose, blood pressure, and blood lipids were assessed.

Aberrant Brain Network Integration and Segregation in Diabetic Peripheral Neuropathy Revealed by Structural Connectomics.

Diabetic peripheral neuropathy (DPN) is one of the most common forms of peripheral neuropathy, and its incidence has been increasing. Mounting evidence has shown that patients with DPN have been associated with widespread alterations in the structure, function and connectivity of the brain, suggesting possible alterations in large-scale brain networks. Using structural covariance networks as well as advanced graph-theory-based computational approaches, we investigated the topological abnormalities of large-scale brain networks for a relatively large sample of patients with DPN ( = 67) compared to matched healthy controls (HCs; = 88).

Sensorimotor and pain-related alterations of the gray matter and white matter in Type 2 diabetic patients with peripheral neuropathy.

Although diabetic peripheral neuropathy (DPN) has long been considered a disease of the peripheral nervous system, recent neuroimaging studies have shown that alterations in the central nervous system may play a crucial role in its pathogenesis. Here, we used surface-based morphometry (SBM) and tract-based spatial statistics (TBSS) to investigate gray matter (GM) and white matter (WM) differences between patients with DPN (n = 67, 44 painless and 23 painful) and healthy controls (HCs; n = 88). Compared with HCs, patients with DPN exhibited GM abnormalities in the pre- and postcentral gyrus and in several deep GM nuclei (caudate, putamen, medial pallidum, thalamus, and ventral nuclear).

The autophagic degradation of Cav-1 contributes to PA-induced apoptosis and inflammation of astrocytes.

The accumulation of palmitic acid (PA), implicated in obesity, can induce apoptotic cell death and inflammation of astrocytes. Caveolin-1 (Cav-1), an essential protein for astrocytes survival, can be degraded by autophagy, which is a double-edge sword that can either promote cell survival or cell death. The aim of this study was to delineate whether the autophagic degradation of Cav-1 is involved in PA-induced apoptosis and inflammation in hippocampal astrocytes.

Waist-to-hip ratio is the most relevant obesity index at each phase of insulin secretion among obese patients.

We aimed to explore the relationship between different obesity indices and insulin secretion at each phase among obese subjects and to find out the most relevant obesity index. Height, weight, waist circumstance, and hip circumstance were obtained among 419 obese subjects to calculate body mass index (BMI), waist-to-hip ratio (WHR), waist-to-height ratio, body adiposity index (BAI), conicity index, abdominal volume index and a body shape index (ABSI). Fasting plasma glucose and fasting insulin were detected to calculate HOMA-β.

High glucose up-regulates Semaphorin 3A expression via the mTOR signaling pathway in keratinocytes: A potential mechanism and therapeutic target for diabetic small fiber neuropathy.

Small fiber neuropathy (SFN) is a common complication in diabetes, and is characterized by decreased intraepidermal nerve fiber density (IENFD). Semaphorin 3A (Sema3A), which is produced by keratinocytes, has a chemorepulsive effect on intraepidermal nerve fibers. mTOR signaling can mediate local protein synthesis that is critical for growth of axons and dendrites.

High glucose induces formation of tau hyperphosphorylation via Cav-1-mTOR pathway: A potential molecular mechanism for diabetes-induced cognitive dysfunction.

The abnormally hyperphosphorylated tau is thought to be implicated in diabetes-associated cognitive deficits. The role of mammalian target of rapamycin (mTOR) / S6 kinase (S6K) signalling in the formation of tau hyperphosphorylation has been previously studied. Caveolin-1 (Cav-1), the essential structure protein of caveolae, promotes neuronal survival and growth, and inhibits glucose metabolism.