Increase In Fasting Blood Glucose Research Articles

Changes in the hippocampal level of tau but not beta-amyloid may mediate anxiety-like behavior improvement ensuing from exercise in diabetic female rats

BackgroundIn the present study, we investigated the effect of high-intensity interval training (HIIT) on cognitive behaviors in female rats with a high-fat diet + streptozotocin (STZ)-induced type 2 diabetes.MethodsTwenty-four female rats were divided into four groups randomly (n = 6): control (C), control + exercise (Co + EX), diabetes mellitus (type 2) (T2D), and diabetes mellitus + exercise (T2D + EX). Diabetes was induced by a two-month high-fat diet and a single dose of STZ (35 mg/kg) in the T2D and T2D + EX groups. The Co + EX and T2D + EX groups performed HIIT for eight weeks (five sessions per week, running on a treadmill at 80–100% of VMax, 4–10 intervals). Elevated plus maze (EPM) and open field test (OFT) were used for assessing anxiety-like behaviors, and passive avoidance test (PAT) and Morris water maze (MWM) were applied for evaluating learning and memory. The hippocampal levels of beta-amyloid (Aβ) and Tau were also assessed using Western blot.ResultsAn increase in fasting blood glucose (FBG), hippocampal level of Tau, and a decrease in the percentage of open arm time (%OAT) as an index of anxiety-like behavior were seen in the female diabetic rats which could be reversed by HIIT. In addition, T2D led to a significant decrease in rearing and grooming in the OFT. No significant difference among groups was seen for the latency time in the PAT and learning and memory in the MWM.ConclusionsHIIT could improve anxiety-like behavior at least in part through changes in hippocampal levels of Tau.

Fasting Blood Glucose: A Mediator of the Association between Estimated Glomerular Filtration Rate and Arterial Stiffness in Japanese Population with Decreased Kidney Function

Introduction: Low estimated glomerular filtration rate (eGFR) is associated with an increased risk of arterial stiffness in participants with kidney damage. It is uncertain whether this association is due to eGFR itself or is mediated by the eGFR-associated increases in fasting blood glucose (FBG). Method: The cross-sectional study included 865 Japanese participants with decreased kidney function, whose eGFR was less than 90 mL/min/1.73 m2, and recruited individuals who received medical healthcare. The mediating variable was FBG, with eGFR as the independent variable and brachial-ankle pulse wave velocity (baPWV) as the dependent variable. A mediation analysis was used to evaluate the mediating effect of FBG on the association between eGFR and arterial stiffness. Results: The mean age of the participants was 51.69 ± 9.25 years old, with 65.90% individuals being male. The mean values for FBG, eGFR, and baPWV were 5.46 ± 0.79 mmol/L, 68.83 ± 10.05 mL/min/1.73 m2, and 1,423.50 ± 247.78 cm/s, respectively. The mediation analysis revealed that eGFR had a significant direct effect on baPWV (β = −25.68 95% CI: −46.42, −7.45), and that FBG played a partial mediating role in the indirect effect of eGFR on baPWV (β = −3.54 95% CI: −11.88, −0.079). Mediation analysis showed that 12.10% of the effect of eGFR on risk of arterial stiffness was mediated through FBG. Conclusion: The study indicated that there is a mediating relationship between eGFR and FBG in people with decreased kidney function, which is associated with the risk of arterial stiffness. Therefore, the importance of FBG as a mediator should be acknowledged and taken into consideration.

Sex-specific effects of a high fat diet on aortic inflammation and dysfunction

Obesity and vascular dysfunction are independent and sexually dimorphic risk factors for cardiovascular disease. A high fat diet (HFD) is often used to model obesity in mice, but the sex-specific effects of this diet on aortic inflammation and function are unclear. Therefore, we characterized the aortic immune cell profile and function in 6-week-old male and female C57BL/6 mice fed a normal chow diet (NCD) or HFD for 10 weeks. Metabolic parameters were measured weekly and fortnightly. At end point, aortic immune cell populations and endothelial function were characterized using flow cytometry and wire myography. HFD-male mice had higher bodyweight, blood cholesterol, fasting blood glucose and plasma insulin levels than NCD mice (P < 0.05). HFD did not alter systolic blood pressure (SBP), glycated hemoglobin or blood triglycerides in either sex. HFD-females had delayed increases in bodyweight with a transient increase in fasting blood glucose at week 8 (P < 0.05). Flow cytometry revealed fewer proinflammatory aortic monocytes in females fed a HFD compared to NCD. HFD did not affect aortic leukocyte populations in males. Conversely, HFD impaired endothelium-dependent vasorelaxation, but only in males. Overall, this highlights biological sex as a key factor determining vascular disease severity in HFD-fed mice.

The combined effects of arteriosclerosis and diabetes on cardiovascular disease risk.

The morbidity and mortality of cardiovascular disease (CVD) rank first among common diseases. Arteriosclerosis and diabetes are risk factors for CVDs, which influence each other. However, their combined effects on CVDs are still unclear. In this study, people who participated in brachial-ankle pulse wave velocity (baPWV) testing and the annual physical examination of the Kailuan Group Finance Co., Ltd., from January 1, 2010, to December 31, 2020, were selected, and their anthropometric, biochemical and epidemiological data were collected. The participants were divided into four groups according to diabetes and arteriosclerosis diagnosis and follow-up. Cox proportional hazards regression and subdistribution hazard models were used to analyse the combined effects of arteriosclerosis and diabetes on CVDs. Multiple sensitivity analyses were also performed. A total of 59,268 Asian populations were selected, including 14,425 females (28.11%) with an average age of 48.10 (± 12.72) years. During follow-up, 1830 subjects developed CVDs (mean follow-up period, 4.72years). The cumulative incidence rates of the healthy control, diabetes, arteriosclerosis, and comorbidity groups were 5.04% (807/38781), 15.17% (253/3860), 17.04% (465/5987), and 25.59% (305/2684), respectively. The results of multivariate Cox regression analysis showed that compared with the healthy control group, the risk of CVD in the diabetes, arteriosclerosis, and comorbidity groups was significantly increased. Their HR values were 1.88 (95% CI 1.62-2.18), 1.40 (95% CI 1.23-1.60), and 2.10 (95% CI 1.80-2.45), respectively. The results of the sensitivity analysis were robust. For each one standard increase in fasting blood glucose or baPWV, the HR values for CVDs were 1.16 (95% CI 1.12-1.20) and 1.22 (95% CI 1.16-1.28), respectively. The results indicated that both arteriosclerosis and diabetes lead to an increased risk of CVDs. The risk of CVDs, coronary atherosclerotic heart disease, heart failure, stroke, coronary artery bypass grafting and ischemic stroke in patients with arteriosclerosis and diabetes was significantly higher than that in patients with arteriosclerosis or diabetes alone. Therefore, the primary prevention of CVDs in patients with arteriosclerosis complicated with diabetes needs more attention.

Trpc6 knockout protects against renal fibrosis by restraining the CN‑NFAT2 signaling pathway in T2DM mice.

Diabetic kidney disease (DKD), one of the common complications of type‑2 diabetes mellitus (T2DM), has become the principal cause of end‑stage kidney disease. Transient receptor potential channel 6 (TRPC6), one of non‑selective cation channels with significant calcium‑permeability, is associated with renal fibrosis. However, the mechanism of TRPC6 in T2DM‑induced renal fibrosis is still not entirely understood. The present study explored the potential mechanism of Trpc6 knockout in T2DM‑induced renal fibrosis in Trpc6‑/‑ mice. The results showed that Trpc6 knockout inhibited the loss of body weight and the increase of fasting blood glucose (FBG) and significantly improved renal dysfunction and glomerular fibrosis in T2DM mice. The present study also indicated that Trpc6 knockout significantly lowered the expression of phosphorylated (p‑)SMAD2/3, TGF‑β, calcineurin (CN), nuclear factor of activated T‑cell (NFAT)2 and Nod‑like receptor (NLR) 3 inflammasome‑associated proteins. Calcium imaging results revealed that Trpc6 knockdown could decrease the levels of [Ca2+]i and inhibited calcium homeostasis imbalance. Moreover, it was found that knockout of Trpc6 had no significant influence on lipid disposition and reactive oxygen species generation in the kidney cortex. The present study suggested that knockout of Trpc6 may alleviate glomerular fibrosis and delay DKD progression by reducing [Ca2+]i overload and inhibiting the CN‑NFAT2 pathway in T2DM mice.

The possible effects of the aqueous extract of Stevia Rebaudiana on autophagic clearance and sympathetic nerve density in pancreatic β cells of type 2 diabetic rats

BackgroundDiabetes mellitus (DM) is a common metabolic disorder affecting more than 400 million people worldwide. Pancreatic islet cell failure due to partial loss or dysfunction of islet cells is a common feature in type 2 DM. The aim of this study to assess the possible protective role of aqueous extract of stevia on pancreatic β cells of type 2 diabetic rats. MethodsThirty-two male Sprague Dawley rats were divided into four groups; control, control received stevia, type 2 DM and type 2 DM treated with stevia. For all groups; fasting blood glucose, fasting insulin, pancreatic Malondialdehyde (MDA) and Catalase (CAT) were measured. Western blot analysis for measuring LC3 (microtubule associated protein-1 light chain-3) and LAMP2 (lysosomal associated membrane protein 2) was done. Also, histopathological, histomorphometric studies and tyrosine hydroxylase (TH) and norepinephrine (NE) expression by immunostaing in pancreatic tissues were detected. ResultsType 2 DM resulted in a significant increase in fasting blood glucose, pancreatic MDA, LC3 and LAMP2 expression, TH and NE density with a significant decrease in fasting insulin, pancreatic CAT, pancreatic islet area, the number of islets per unit area and the number of β cell per islet. Also, treatment with stevia extract significantly improved the laboratory and histopathological features of pancreas ConclusionStevia extract has protective effects on type 2 DM pancreas by its hypoglycemic and antioxidant actions in addition to its ability to attenuate hyperactive autophagy and sympathetic nerve density.

Effects of Kudzu Root on Oxidative Stress and Inflammation in Streptozotocin-induced Diabetic Rats

Background: Oxidative stress and inflammation are strictly connected, and both perform an important role in the pathogenesis of diabetes mellitus (DM). Objectives: This research aimed to investigate the potential protective effect of kudzu root against oxidative stress and inflammation in a streptozotocin (STZ)-induced DM animal model. Methods: DM was induced in male Wistar rats by intraperitoneal injection of STZ (50 mg/kg body weight). The kudzu root (100 mg/kg BW) was administered orally after 1 week of STZ administration in diabetic animals (for 6 weeks). Results: The diabetic animals exhibited a significant increase in fasting blood glucose, tumor necrosis factor-alpha, and malondialdehyde levels. However, they exhibited a significant decrease in plasma insulin level, superoxide dismutase, and glutathione peroxidase activity. Administration of kudzu root to diabetic animals reversed these effects. Conclusion: The current study indicated that kudzu root has potent antidiabetic properties, likely through its anti-inflammatory and anti-oxidative properties in the STZ-diabetic rat model.

Effects of pemafibrate on left ventricular diastolic function in patients with type 2 diabetes mellitus: a pilot study.

Diabetic cardiomyopathy (DCM) is characterized predominantly by diastolic dysfunction. The multiple mechanisms underlying DCM include altered energy substrate utilization. Recent studies indicate that PPARα plays an important role in the pathogenesis of lipotoxic cardiomyopathy. Pemafibrate is known to be a selective PPARα modulator (SPPARMα). We thus investigated the effects of pemafibrate on cardiac diastolic function in patients with type 2 diabetes. Seventeen patients with type 2 diabetes (T2D) and hypertriglyceridemia were screened and treated with pemafibrate at a dose of 0.2mg/day for 8-16weeks. Fourteen patients were eligible for analysis. Echocardiography was used for assessment of diastolic function. Early diastolic filling velocity (E), late atrial filling velocity (A) and the E/A ratio were included in this study. Peak early diastolic annular velocities (e') were also assessed using color tissue Doppler images. The primary endpoints were changes in the ratio of E to A (E/A), e', and the ratio of E to e' (E/e') from baseline. Pemafibrate significantly increased average e' (7.24 ± 0.58 vs 7.94 ± 0.67, p = 0.019) and a significant reduction in E/e' (9.01 ± 0.94 vs 8.20 ± 0.91, p = 0.041). The increase in e' was significantly related to increases in fasting blood glucose (r = 0.607, p = 0.021) and non-esterified fatty acid (r = 0.592, p = 0.026). Pemafibrate improved diastolic function in patients with T2D and hypertriglyceridemia, suggesting that PPARα activation by pemafibrate prevents the development of DCM at an early stage.

Investigation of Cyclo-Z Therapeutic Effect on Insulin Pathway in Alzheimer's Rat Model: Biochemical and Electrophysiological Parameters

Cyclo (his-pro-CHP) plus zinc (Zn+2) (Cyclo-Z) is the only known chemical that increases the production of insulin-degrading enzyme (IDE) and decreases the number of inactive insulin fragments in cells. The aim of the present study was to systematically characterize the effects of Cyclo-Z on the insulin pathway, memory functions, and brain oscillations in the Alzheimer's disease (AD) rat model. The rat model of AD was established by bilateral injection of Aβ42 oligomer (2,5nmol/10μl) into the lateral ventricles. Cyclo-Z (10mg Zn+2/kg and 0.2mg CHP/kg) gavage treatment started seven days after Aβ injection and lasted for 21 days. At the end of the experimental period, memory tests and electrophysiological recordings were performed, which were followed by the biochemical analysis. Aβ42 oligomers led to a significant increase in fasting blood glucose, serum insulin, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) and phospho-tau-Ser356 levels. Moreover, Aβ42 oligomers caused a significant decrement in body weight, hippocampal insulin, brain insulin receptor substrate (IRS-Ser612), and glycogen synthase kinase-3 beta (GSK-3β) levels. Also, Aβ42 oligomers resulted in a significant reduction in memory. The Cyclo-Z treatment prevented the observed alterations in the ADZ group except for phospho-tau levels and attenuated the increased Aβ42 oligomer levels in the ADZ group. We also found that the Aβ42 oligomer decreased the left temporal spindle and delta power during ketamine anesthesia. Cyclo-Z treatment reversed the Aβ42 oligomer-related alterations in the left temporal spindle power. Cyclo-Z prevents Aβ oligomer-induced changes in the insulin pathway and amyloid toxicity, and may contribute to the improvement of memory deficits and neural network dynamics in this rat model.

Long-term increase in fasting blood glucose is associated with increased risk of sudden cardiac arrest

BackgroundDiabetes mellitus (DM) is associated with various cardiovascular complications, including sudden cardiac arrest (SCA). Furthermore, the severity of DM, as assessed by fasting blood glucose (FBG), is associated with the risk of SCA. However, whether long-term changes in FBG influence on SCA risk remains to be determined.MethodsThis study used sequential nationwide health screening data from 2009 and 2011. FBG was measured at each health screening, and ΔFBG was calculated as FBG in 2011–FBG in 2009.ResultsOverall, 2,801,153 people were analyzed, and the mean follow-up duration was 6.33 years. Compared with the euglycemic group (− 20 ≤ ΔFBG < 20), the 20 ≤ ΔFBG < 40, 40 ≤ ΔFBG < 100, and ΔFBG ≥ 100 groups had increased SCA risks of 25% (adjusted hazard ratio [HR] = 1.25; 95% confidence interval [CI] 1.16–1.35; p < 0.001), 66% (adjusted HR = 1.66; 95% CI 1.49–1.86; p < 0.001), and 2.9-fold (adjusted HR = 2.85; 95% CI 2.37–3.44; p < 0.001), respectively. The association between ΔFBG and SCA was maintained in people with DM but not in people without DM. However, sex, age, blood pressure, and presence of heart failure did not affect the association between ΔFBG and SCA. A decrease in ΔFBG over time was not associated with reduced risk of SCA: the adjusted HR was 1.11 (95% CI 0.98–1.27; p = 0.113) for the ΔFBG < –40 group and 1.12 (95% CI 1.03–1.22; p = 0.009) for the − 40 ≤ ∆FBG < − 20 group.ConclusionsA long-term increase in ΔFBG can be associated with increased risk of SCA in people with DM. However, a long-term decrease in ΔFBG was not associated with reduced risk of SCA. Actions to prevent increase in FBG can have significant effects on public health in terms of SCA prevention.

Trpc6 knockout improves behavioral dysfunction and reduces Aβ production by inhibiting CN-NFAT1 signaling in T2DM mice

As the prevalence of diabetes and health awareness increase, type 2 diabetes mellitus -associated cognitive dysfunction is receiving increasing attention. However, the pathogenesis is not entirely understood. Transient receptor potential cation channel 6 (TRPC6) is highly correlated with intracellular Ca2+ concentrations, and neuronal calcium overload is an important cause of cognitive dysfunction. In the present study, we investigated the effect and mechanism of Trpc6 knockout in high-fat diet and streptozotocin-induced T2DM mice. The body weight and fasting blood glucose were recorded during the experiment. Behavioral dysfunction was detected using the open field test (OFT), elevated plus maze (EPM), hole-board test (HBT), Morris water maze (MWM) test and contextual fear conditioning (CFC) test. Nissl and H&E staining were used to examine neuronal damage. Western blot, quantitative real-time polymerase chain reaction (q-PCR), and immunofluorescence were performed to detect amyloid beta protein (Aβ) deposition and related indicators of neurological impairments in the cerebral cortex and hippocampus. The results indicated that Trpc6 knockout inhibited body weight loss and fasting blood glucose increase, improved spontaneous activity, learning and memory dysfunction, and alleviated neuroinflammation and neuronal damage in T2DM mice. The further results demonstrated that Trpc6 knockout decreased Aβ generation and deposition, and reduced the expressions of inflammasome-related proteins in T2DM mice. In addition, Trpc6 knockout inhibited intracellular calcium overload in diabetic mice and primary cultured hippocampal neurons, which in turn suppressed CN and NFAT1 expression. These data suggest that Trpc6 knockout may inhibit the CN-NFAT1 signaling pathway by decreasing intracellular calcium overload in the brain of T2DM mice, which consequently reduce Aβ deposition and neuroinflammation, and ultimately delay the development of T2DM-associated cognitive dysfunction.

Different Doses of Lumbar Epidermal Methylprednisolone Injection and their effect on Pain Control and Blood Glucose Level in Diabetic patients

Background: Frequency of diabetes mellitus is high between people suffering from lumbar spinal degenerative sickness Despite the fact that injection of steroid in epidural space are recognised to rise the glycaemic Blood amount postoperatively, therefore it is inquiry that decrease dose of methylprednisolone (40mg) cannot rise blood glycaemic level as compare to higher dose of methylprednisolone (80mg) and their effect on pain management of patients. Aim: To evaluate 2 common doses (80mg &amp; 40mg) of methylprednisolone effects which is given through Epidural lumbar route, on glycaemic Blood level and pain management of diabetes mellitus patients to determine an adequate epidural steroid dose. Methods: This was an observational prospective study was conduct at Department of Anaesthesia Hayatabad Medical Complex Peshawar in June 2022. Overall 110 Diabetes mellitus patients were participated. They acquired lumbar epidural, methylprednisolone for spinal stenosis radiculopathy or failed back surgery syndrome. Methylprednisolone dose were given to patients, either 80mg (Group A) or 40 mg (Group B) was determined clinically after the procedure type. Results: HbA1c level was noted in group A 6.21mmol/L while in group B 6.52 mmol/L (p =0.991). The increase in fasting blood glucose (FBG) were greater significantly A Group than in B Group on post procedure day (PPD)1,2&amp;3 (PPD1: 179 mg/dL A Group Vs 146mg/dL in B Group ), (PPD2: 221 mg/dL in A Group Vs 152mg/dL in B Group ) &amp; (PPD3: 202mg/dL in A Group Vs 175mg/dL in B Group ). Fasting blood glucose incidence was &gt;180mg/dL were greater in A Group than in B Group on post procedure day 1&amp;2 (PPD1: A Group=11 vs B Group=5) and (PPD2: A Group=13 Vs B Group= 4). Conclusion: Methylprednisolone increase dose 80mg rise FBG and PDG greater than a decrease dose 40mg with no effect on pain management, employment status, or clinical outcome. Thus, it is recommended that methylprednisolone 40mg will b given rather than 80mg in diabetes mellitus patients with respect to pain management and blood glycaemic level Keywords: Epidural methylprednisolone, back pain, blood glucose.

Investigation of the effects of swimming exercises in rats given acrylamide

Acrylamide is a toxic substance used in industrial and laboratory processes. Acrylamide exposure has a toxic effect on many systems. Protective mechanisms should be developed against the effects caused by acrylamide. In our study, we investigated whether exercise has a protective effect against the changes that acrylamide will cause in pancreas. 32 adult Sprague-Dawley male rats were used. Control group was given only saline. Exercise group was applied swimming exercise for 1hour daily for 4 weeks. Acrylamide group was given 50mg/kg acrylamide by gavage for 4 weeks. Acrylamide+exercise group was applied 50mg/kg acrylamide for 4 weeks and swimming exercise for 1hour daily. After the experiment, fasting blood glucose and oral glucose tolerance test measurements were performed. Then, blood and pancreas samples were taken. Acrylamide exposure caused an increase in fasting blood glucose and oral glucose tolerance, a decrease in insulin levels and oxidative stress in acrylamide group. In exercise group, these values were similar to control group and no significant change was observed in acrylamide+exercise group. While there was an increase in the number of alpha cells in acrylamide group compared to the other groups, here was a decrease in the number of beta cells compared to control group. We can say that acrylamide causes changes in the islets of Langerhans by affecting alpha and beta cell numbers. The protective effect of exercise on beta and alpha cell mass was not statistically significant in the acrylamide+exercise group. When the results were examined, the decrease in oxidative stress and the higher number of beta and alpha cells in the acrylamide+exercise group compared to the acrylamide group suggested that 4 weeks of swimming exercise may have an effect on acrylamide exposure.

Age patterns of nonalcoholic fatty liver disease incidence: heterogeneous associations with metabolic changes

BackgroundAs the nonalcoholic fatty liver disease (NAFLD) epidemic matures, understanding how metabolic changes in NAFLD development vary over the age distribution is important to guide precise prevention. We aimed to clarify metabolic trends in age-specific NAFLD incidence.MethodsWe conducted a 4-year longitudinal retrospective cohort study enrolling 10,240 consecutive healthy individuals who received annual physical examination during 2012–2019. Baseline and dynamic changes in metabolism and hepatic steatosis determined with ultrasound were collected and analyzed stratified by age into the following groups: 20–34, 35–49, 50–64, and over 65 years.ResultsOverall, 1701 incident NAFLD participants (16.6%) were identified. Adjusted Cox regression analysis showed that the baseline and increased body mass index were the main risk factors for NAFLD in people ≤ 65 years old. Baseline high-density lipoprotein (HR = 0.56; 95% CI 0.39–0.78) was a protective factor for newly onset NAFLD in the 50-to-64-year-old group, while baseline SBP (HR = 1.03; 95% CI 1.01–1.05), baseline uric acid (HR = 1.04; 95% CI 1.01–1.07), triglyceride increase (HR = 4.76; 95% CI 3.69–6.14), fasting blood glucose increase (HR = 1.32; 95% CI 1.06–1.65) were independently associated with incident NAFLD in over-65-year-old group.ConclusionsNAFLD incidence attributable to potentially metabolic risk factors varied substantially across age groups in a cohort of Chinese people. The adoption of age targeted metabolic prevention strategies might reduce the burden of NAFLD.

The functions of SID1 transmembrane family, member 2 (Sidt2).

The SID1 transmembrane family, member 2, namely, Sidt2, is a highly glycosylated multichannel lysosomal transmembrane protein, but its specific physiological function remains unknown. Lysosomal membrane proteins are very important for the executive functioning of lysosomes. As an important part of the lysosomal membrane, Sidt2 can maintain the normal morphology of lysosomes and help stabilize them from the acidic pH environment within. As a receptor/transporter, it binds and transports nucleic acids and mediates the uptake and degradation of RNA and DNA by the lysosome. During glucose metabolism, deletion of Sidt2 can cause an increase in fasting blood glucose and the impairment of grape tolerance, which is closely related to the secretion of insulin. During lipid metabolism, the loss of Sidt2 can cause hepatic steatosis and lipid metabolism disorders and can also play a role in signal regulation and transport. Here, we review the function of the lysosomal membrane protein Sidt2, and focus on its role in glucose and lipid metabolism, autophagy and nucleotide (DNA/RNA) transport.

Elevated IL-31 and IL-31RA with dyslipidemia in T2DM patients

Type 2 Diabetes mellitus (T2DM) is characterized by elevated of blood glucose, and considered as a chronic metabolic disease. Uncontrolled blood glucose levels cause many dangerous complications. One of these complications are diabetic foot ulcers (DFU). About 15% of these patients suffering of DFU that affected on their lives. Approximately 8.5% Iraqi suffer from T2DM. Sixty T2DM patients (32 male and 28 female) aged 39-65 years that participated in the present study. Thirty apparently healthy subjects (12 male and 18 female) were classified as a control group. Age and BMI are not significantly different between patients and controls. This was made to exclude the influence of body mass and age on the results. There is an expected significant increase in fasting blood glucose (FBG) (p &lt;0.001) and glycated hemoglobin (HbA1c). The results showed a significant increase (p&lt;0.001) in serum triglyceride (TG), VLDLc in T2DM as comparison with the control group, while There were no significant differences among T2DM patients and control group in total cholesterol (TC), HDLc and LDLc. This result maybe was by the effect of diabetic drug on lipid profile where some drugs such as metformin that reducing cholesterol.

Diabetes and COVID-19: Biological profile of type 2 diabetic patients with COVID-19 in Pointe-Noire, Congo

Introduction: COVID-19 is new pneumonia caused by SARS-CoV-2 infection. Several factors of bad prognosis have been implicated including diabetes. Several poor prognostic factors have been associated with the severity of this disease, including diabetes. In Congo, no study to date has investigated the profile of diabetics hospitalized for COVID-19. The aim of this study was to evaluate the biological profile of Congolese diabetic patients admitted to the hospital for COVID-19 in Pointe-Noire. Materials and methods: This was a prospective study conducted among patients hospitalized for COVID-19 in Pointe-Noire between March and November 2020. Sociodemographic, clinical and biological data, duration of hospitalization, and viral load were investigated. A total of 84 COVID-19 patients have been admitted to Louise Michel Clinic and the Adolph Sice General Public Hospital. Two groups were formed: diabetic patients and non-diabetic patients based on the history of antidiabetic medication or fasting plasma blood glucose levels at admission. Results between the two groups were compared. Results: Out of 84 COVID-19 patients, 48 were diabetic (mean age: 48.50 ± 11.98 years) versus 36 non-diabetic (mean age: 45.56 ± 8.48 years). Significant increases in fasting blood glucose, D-dimers, white blood cells, low oxygen saturation (SaPO2), and higher mortality was observed were observed in COVID-19-positive diabetics when compared to non-diabetic patients(p &lt; 0.02). However, no significant differences were observed between the two groups in terms of clinical symptoms. An increased risk of death was associated with higher levels of D-dimers and HbA1c at admission in the diabetic group. Conclusion: An increase in D-dimer levels and high blood glucose levels at admission increased the risk of death in diabetic patients with COVID-19 in Pointe-Noire.

1518-PUB: Role of PPARd in Regulating Autophagy Pathway in Improving Islet ß-Cell Function with GLP-1 Receptor Agonist

Aim: To investigate the effect and mechanism of glucagon-like peptide-1 receptor agonist (GLP-1 RA) on the function of islet β cells. Methods: Type 2 diabetes C57BL/6J mice were successfully induced by high fat diet (HFD) feeding for 12 weeks then were randomly divided into HFD+NaCl group (n=5) , HFD+Exenatide group (n=5, 24 nmol•kg-1­•d‑1) and NC group (n=5) . Tolerance tests and insulin measurement were performed after 8 weeks of drug therapy. Weight was measured weekly and fasting blood glucose was measured every 4 weeks. The pancreas were stained with LC3B Immunofluorescence at the end of the experiment. The PA induced primary islet β cells were treated with exendin-4 and PA induced Min6 cells were treated with exendin-4, GW501516 for 24h, which BSA as the control group, then detected the protein levels of PPARδ, LC3B-II and P62. At the same time, PA induced MIN6 cells were treated with GSIS. What's more, we silenced PPARδ transfected with siRNA to verify the role of PPARδ in GLP-1 receptor agonist activation of β-cell autophagy. Results: Compared with the normal control group, the body weight and fasting blood glucose increase and significant peripheral insulin resistance in the high fat group, while the above indexes are significantly improved in the high-fat fed mice after GLP-1 RA treatment. Immunofluorescence biopsies of pancreatic tissue show that LC3B expression decrease after high fat diet, while GLP-1 RA intervention significantly increase. In addition, GLP-1 RA not only can promote the expression of PPARδ and LC3B-II protein and inhibit the expression of P62 protein in primary islet β cells and MIN6 cells, but also significantly increase glucose stimulation insulin secretion in MIN6 cells. More importantly, GW501516 is found to be consistent with GLP-1 RA in MIN6 cells, while GLP-1 RA promote autophagy disappeare after PPARδ expression is silenced. Conclusion: GLP-1 RA can improve the function of islet β cells by activating the autophagy pathway through PPARδ. Disclosure Y.Su: None. B.Lin: None. Y.Chen: None. Z.Liu: None. L.Gan: None. W.Xu: None. Funding Science &amp; Technology Project of Guangzhou（202102010175）

The contribution of avoidable factors in doubling or halving the odds of hypertension

Despite the well-known impact of fruit/vegetable consumption, physical activity, body mass index, waist-hip ratio, fasting blood glucose, and total cholesterol on blood pressure, the amount of exposure to these factors is required to halve or double the odds of hypertension is unknown, but it was investigated in this research. The data used in this study are derived from results of the seventh Iranian national STEPS survey involving 30,542 adults aged 18 years or older. The questionnaire measured non-communicable disease risk factors covered three different levels including behavioral characteristics, physical and biochemical measurements. The level of exposure to factors necessary to reach the odds ratio of 0.5 or odds ratio of 2.0 was obtained from the coefficients of the multiple logistic regression model. An OR of 0.5 corresponds to 7 servings of fruit and vegetable consumption daily and burning of 7175 kcal through physical activity at work or recreation daily. An OR of 2.0 corresponds to an increase in body mass index of about 11 kg/m2, an increase in the waist-hip ratio of about 18%, an increase in fasting blood glucose of about 77 mg/dl, and an increase in total cholesterol of about 134 mg/dl. The results of this study indicate how much fruit and vegetable and physical activity halve the odds of hypertension and how much increase in body mass index, the waist-hip ratio, fasting blood glucose, and total cholesterol can double the odds of hypertension. Such information may be useful for developing guidelines by policymakers.

Dietary Advanced Glycation End Products Shift the Gut Microbiota Composition and Induce Insulin Resistance in Mice.

ObjectiveThis study aimed to explore the associations between gut microbiota characteristics and glycometabolic profiles in mice fed diets high in advanced glycation end products (AGEs).MethodsC57BL/6 mice were exposed to a heat-treated diet or exogenous AGEs for 24 weeks, and glucose metabolism was assessed via the intraperitoneal glucose-tolerance test (IPGTT). Serum AGE and lipopolysaccharide-binding protein (LBP) levels were quantified using ELISA kits. 16S rDNA sequencing was performed to analyze the changes in gut microbiota according to α- and β-diversity. Key operational taxonomic units (OTUs) were evaluated, and co-abundance groups (CAGs) were delineated using weighted correlation network analysis. Associations between CAGs and clinical parameters were analyzed using Spearman correlation; predictive functional analysis of gut microbiota was performed using Kyoto Encyclopedia of Genes and Genomes data.ResultsWe identified significant increases in fasting blood glucose (FBG) and fasting insulin levels, as well as homeostatic model assessment insulin resistance (HOMA-IR) and glucose area under the receiver operating characteristic curve from IPGTT, in the high-AGE diet groups relative to controls at week 24. Serum AGE and LBP levels were elevated, and the α- and β-diversity of gut microbiota reduced in high-AGE diet groups. We identified 92 key OTUs that clustered into six CAGs, revealing positive correlations between CAG2/3/5 and insulin levels and mice weight and negative correlations between CAG1/3/4/5 and AGE, FBG, and LBP levels and HOMA-IR in mice fed high-AGE diets. We observed a reduced abundance of butyrate-producing bacteria, including Bacteroidales_S24-7, Ruminococcaceae, and Lachnospiraceae, in mice fed high-AGE diets, with pathway analysis of gut microbiota revealing significantly enriched fructose and mannose metabolism.ConclusionHigh-AGE diets altered the gut microbiota composition and structure, and induced insulin resistance in mice. In the pathogenesis of insulin resistance, the loss of butyrate-producing bacteria might impair the colonic epithelial barrier, thereby triggering chronic low-grade inflammation.