WoodMimicking BioBased Biporous Polymeric Components along with Anisotropic Tubular Macropores

This study aimed to identify the prevalence and gender differences of metabolic syndrome in young new-onset ketosis-prone type 2 diabetic (KPT2D) individuals.
A retrospective study was conducted in Shanghai Xin Hua Hospital from 2007 to 2019. A total of 304 patients from 12 to 40 years of age with newly diagnosed diabetes presenting with ketosis were analyzed. The clinical features and laboratory results of KPT2D and type 1 diabetic (T1D) individuals were compared. Prevalence and gender differences of metabolic syndrome in the KPT2D subjects were analyzed.
The prevalence of metabolic syndrome (
< 0.0001) was significantly higher in young KPT2D than T1D subjects. The prevalence of high blood pressure (
< 0.0001), central obesity (
< 0.0001), low plasma HDL-C concentration (
= 0.045), and hypertriglyceridemia (
< 0.0001) was elevated in the KPT2D subjects compared with T1D. Male predominance (89%) was presented in the KPT2D subjects. The prevalence of metabolic syndrome (
= 0.0002) was significantly higher in young male than female KPT2D subjects. The presence of central obesity (
< 0.0001) and high blood pressure (
=0.03) was higher in male KPT2D subjects than female. The presence of serum triglyceride concentrations ≥ 2.3mmol/L was significantly higher (
= 0.011) in male KPT2D subjects than female.
Significantly higher prevalence of metabolic syndrome in young KPT2D patients compared with T1D patients could be an important reference for diabetic differential diagnosis. KPT2D presented a higher predominance in young males, who had higher prevalence of metabolic syndrome than young females.
Significantly higher prevalence of metabolic syndrome in young KPT2D patients compared with T1D patients could be an important reference for diabetic differential diagnosis. KPT2D presented a higher predominance in young males, who had higher prevalence of metabolic syndrome than young females.
Cardiovascular disease can be detected in individuals with prediabetes. The purpose of this study was to determine whether soluble suppression of tumorigenicity 2 (sST2), which is elevated in cardiovascular disease and/or type 2 diabetes, is correlated with glycated haemoglobin in individuals with glycemia in the normal/prediabetes range.
The anthropometric, biochemical and metabolic parameters were measured in 30 adults, and the plasma levels of sST2 were quantified.
sST2 was directly correlated with glycated hemoglobin in individuals with glycemia in the normal/prediabetes range. Participants who were at the higher end of glycated hemoglobin (5.8-6.4%) had significantly higher sST2 compared to those at the lower end (≤5.5%). Moreover, sST2 was directly correlated with homeostatic model assessment of insulin resistance (HOMA-IR), alkaline phosphatase, and waist circumference. However, the correlation between sST2 and HOMA-IR or waist circumference was lost after adjusting for age, gender or body mass index.
Circulating sST2 may be used to establish a cut-off value for cardiometabolic risk/disease in individuals with glycemia in the normal/prediabetes range.
Circulating sST2 may be used to establish a cut-off value for cardiometabolic risk/disease in individuals with glycemia in the normal/prediabetes range.
Glucagon-like peptide-1 (GLP1) is known to decrease glucagon release and may be beneficial for the reduction of elevated blood glucose. However, its role and mechanism of action in diabetes remain elusive. This study aimed to examine the function of GLP1 and analyze the mechanism of effect that GLP1exerts on inducible nitric oxide synthase (iNOS) in diabetic mice.
A diabetes model was established in ApoE
mice fed a high-fat diet and treated with GLP1 and/or lentivirus-expressing PARP1. PARP1, iNOS, and inflammatory factors in islets were detected by Western blot and ELISA. Islet α cells and β cells and CD8
T lymphocytes were detected by immunostaining. Islet-cell apoptosis was detected by TUNEL.
GLP1 inhibited the expression of PARP1 and iNOS in islets, alleviated decrease in β cells, and suppressed cell apoptosis induced by the high-fat diet. Moreover, GLP1 recovered the decline in insulin sensitivity and glucose tolerance in ApoE
mice fed the high-fat diet, and the effects of GLP1 were related to the inhibition of COX2 and NFκB expression.
GLP1 significantly alleviated the decrease in β-cell numbers, suppressed β-cell apoptosis induced by the high-fat diet, inhibited the expression of iNOS, and alleviated inflammatory islet injury via inhibiting the COX2-NFκB pathway.
GLP1 significantly alleviated the decrease in β-cell numbers, suppressed β-cell apoptosis induced by the high-fat diet, inhibited the expression of iNOS, and alleviated inflammatory islet injury via inhibiting the COX2-NFκB pathway.
In humans, single nucleotide polymorphisms (SNPs) near the adjacent protein kinase D1 (
) and G2/M-phase-specific E3 ubiquitin protein ligase (
) genes on chromosome 14 are associated with obesity. To date, no published evidence links inactivation of either gene to changes in body fat. These two genes are also adjacent on mouse chromosome 12. Because obesity genes are highly conserved between humans and mice, we analyzed body fat in adult
and
knockout (KO) mice to determine whether inactivating either gene leads to obesity in mice and, by inference, probably in humans.
The
and
KO lines were generated by gene trapping and by homologous recombination methodologies, respectively. Body fat was measured by DEXA in adult mice fed chow from weaning and by QMR in a separate cohort of mice fed high-fat diet (HFD) from weaning. Glucose homeostasis was evaluated with oral glucose tolerance tests (OGTTs) performed on adult mice fed HFD from weaning.
Body fat was increased in multiple cohorts of
KO that decrease the amount of functional human G2E3.
TNF-α, a proinflammatory cytokine secreted by activated immune cells, and overexpression of it in adipocytes, has an important role in insulin resistance progression and diabetes development.
Subcutaneous adipocytes derived from mesenchymal stem cells were used for in vitro analysis to find the role of antidiabetic drugs on TNF-α in high glucose-fed adipocytes.
In vitro adipocytes were used along with variable concentration of anti-diabetic drugs. The level of TNF-α was measured by ELISA and the mRNA level was quantified using SYBR-Green real-time PCR. All data were statistically analyzed.
The level of TNF-α and the mRNA expression were observed and analyzed with normal adipocytes. TNF-α level and expression of it showed agonistic behavior, ie no change at low concentration while enhances with the increase of glucose. The level was decreased significantly when the adipocytes were treated with metformin (
=0.015) and pioglitazone (
=0.020). Tirzepatide A combination of drugs showed that the expression of TNF-α was almost the same as for metformin alone.