Our results indicate that high-glucose load leads to glucose intolerance with insulin resistance through impairment of GLP-1 secretion, increase of blood glucose levels via activating TLR4 and increasing levels of IL-6 and TNF-α in mice.
We found that heat-killed <i>S. thermophilus</i> treatment reduced fasting blood glucose levels and alleviated glucose intolerance and total cholesterol in diabetic ZDF rats.Additionally, heat-killed <i>S. thermophilus</i> increased the interleukin 10 while reducing the levels of lipopolysaccharide, interleukin 6, and tumor necrosis factor-α in diabetic ZDF rats.The heat-killed <i>S. thermophilus</i> treatment can normalize the structure of the intestinal and colon mucosal layer of diabetic rats.
The results showed that PJE reduced insulin resistance and glucose intolerance, decreased hepatic lipid accumulation, and inflammatory markers such as PPARγ and TNFα, respectively.
However, PCE did protect against dyslipidemia, fasting hyperglycemia, and glucose intolerance, and attenuated both hepatic gluconeogenesis and inflammation as observed by the expression of tumor necrosis factor-α and transcriptional factor NF-κB.
Glucose intolerance was partially prevented by <i>L. kefiri</i> treatment (GTT) and local inflammation (TNFα; IL1β; IL6 and INFγ) was completely inhibited in EAT.<i>L. kefiri</i> supplementation generated an impact on gut microbiota composition, changing <i>Bacteroidetes</i> and <i>Firmicutes</i> profiles.
Elevated levels of the cardiac inflammatory cytokines IL-6 and TNFα leading to impaired insulin signalling may partially explain the peripheral glucose intolerance.
In acinar cells, our study demonstrates an age-associated Arg-II upregulation, which promotes TNF-α release through p38 MAPK leading to β-cell apoptosis, insufficient insulin secretion, and glucose intolerance in female rather than male mice.
As expected, a lard-based, very high-fat diet (60% energy) significantly increased adiposity and glucose intolerance compared with 10% fat-fed controls, coincident with higher retroperitoneal (RP) WAT transcript levels for proinflammatory factors and macrophage markers, including TNFα and CD68 mRNA, which were ~3- and ~15-fold of control levels, respectively (P < 0.001).
Compared to NGT group, interleukin-6, tumor necrosis factor-alpha (TNF-alpha), p(22)Phox NADPH oxidase, and thioredoxin interacting protein (TXNIP) mRNA levels were higher and suppressor of cytokine signaling (SOCS-3) mRNA was lower in subjects with IGT and diabetes.
Single nucleotide polymorphisms (SNPs) in the ADRB2, ADRB3, TNF, IL6, IGF1R, LIPC, LEPR, and GHRL genes were associated with the conversion from impaired glucose tolerance (IGT) to type 2 diabetes mellitus (T2D) in the Finnish Diabetes Prevention Study (DPS).
Our findings are the first to indicate that a higher incidence of impaired glucose tolerance and low circulating adiponectin concentration may be associated with interaction between the -308G/A promoter polymorphism of the TNF-alpha gene and SNP 45 in the adiponectin gene.
We conclude that the -308A allele of the promoter polymorphism (G-308A) of the TNF-alpha gene is a predictor for the conversion from IGT to type 2 diabetes.
The prevalence of the 238, but not of the 308, TNF-alpha polymorphism was higher in subjects with nonalcoholic fatty liver than in controls (31% vs. 15%; P < 0.0001), and patients positive for TNF-alpha polymorphisms had higher insulin resistance indices, a higher prevalence of impaired glucose tolerance, and a lower number of associated risk factors for steatosis.
The aim of this study was to investigate the mRNA expression pattern of the two TNF receptors and their ligand in two adipose tissue depots of glucose-tolerant obese women [n = 18, body mass index (BMI) 48.2 +/- 8.4 kg m-2], obese women with impaired glucose tolerance or overt non-insulin-dependent diabetes mellitus (NIDDM) (n = 10, BMI 49.1 +/- 11.6 kg m-2) and healthy non-obese control subjects (n = 12, BMI 25.8 +/- 2.7 kg m-2).