Disturbed islet architecture has been proposed as the reason why mice with complete inactivation of paired box 6 (PAX6) in the pancreas develop diabetes.
After adjustment for age, gender, duration of diabetes, and BMI, multivariate analysis showed significant association of smoking (<i>p</i>=0.002) and HOMA-IR (<i>p</i>=0.003) with intraocular IL-6 levels, while intraocular VEGF and systemic Lp-A levels correlated significantly (<i>p</i>=0.032).
In this biracial cohort, elevated lipoprotein(a) levels in Caucasian individuals with diabetes or prediabetes were associated with further increased ASCVD risk.
In addition to its recently recognized role in diabetes, aberrant TCF7L2 expression has been implicated in cancer through regulation of cell proliferation and apoptosis by c-MYC and cyclin D. It has been hypothesized that germline variants within the TCF7L2 gene previously associated with diabetes may affect cancer risk through the Wnt/beta-catenin signaling pathway.
In this issue of the JCI, Lyssenko and colleagues report on their human and isolated islet studies and suggest that the risk allele increases TCF7L2 expression in the pancreatic beta cell, reducing insulin secretion and hence predisposing the individual to diabetes (see the related article beginning on page 2155).
Our findings thus propose a potential cellular mechanism through which abnormal TCF7L2 activity predisposes individuals to diabetes and implicates abnormalities in the islet microenvironment in this disease.
Our study demonstrates that CHD and periodontitis are genetically related by at least one susceptibility locus, which is possibly involved in ANRIL activity and independent of diabetes associated risk variants within this region.
The serum levels of these factors were also analyzed in patients with diabetes and no diabetic retinopathy (NDR) and with non-proliferative diabetic retinopathy (NPDR), to detect the possible correlation between the ANGPTL-8 levels and hyperlipidemia.
This study shows for the first time in an in vivo model of diabetes that GLO-I overexpression reduces hyperglycemia-induced levels of carbonyl stress, AGEs, and oxidative stress.
HIF-1alpha overexpression also normalized diabetes-reduced vascular endothelial growth factor concentration along with a sustained myocardial capillary density and an inhibition of cardiomyocyte hypertrophy and cardiac fibrosis.
These findings indicate that GPR120 activation is protective against lipotoxicity-induced pancreatic β-cell dysfunction, via the mediation of PDX1 expression and inhibition of islet inflammation, and that GPR120 activation may serve as a preventative and therapeutic target for obesity and diabetes.
In late postmenopausal women, lower OC and CTX levels were associated with similarly increased risks of insulin resistance at baseline and incident diabetes over long-term follow-up.
Mutations in the transcription factors HNF1A and HNF4A and in the β-cell potassium ATP channel components cause diabetes which responds to low dose and high dose sulfonylurea agents, respectively, while glucokinase mutations require no treatment.
A decrease in VEGF and nephrin could be validated at the protein level and also at the RNA level in renal biopsy specimens from 5 additional patients with diabetes.
These studies highlight the clear, and persistent, metabolic advantages of sustained activation of GLP-1 receptors, alongside concurrent activation of related GIP and xenin cell signalling pathways, in diabetes.
The hypothesis tested is that expression of VEGF, considered the effective cytokine in the relationship between diabetes and periodontal disease, is differentially affected in gingivitis and periodontitis patients with or without diabetes mellitus compared to healthy controls.