Increase In Fasting Blood Glucose Research Articles

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.

Turmeric extract alleviates endocrine-metabolic disturbances in letrozole-induced PCOS by increasing adiponectin circulation: A comparison with Metformin

One of the most common causes of female infertility is polycystic ovarian syndrome, which affects 6–21% of the population. Regrettably, the currently available treatments are mostly symptomatic and ineffective. As a result, safer options are needed now more than ever. In a letrozole PCOS albino mouse model, the current study compares the therapeutic advantages of Turmeric extract (Curcuma longa) to metformin. Adiponectin is a circulating protein generated by adipocytes that has been linked to metabolic diseases (MDs) in an inverse relationship. The effects of Turmeric Extract (Curcuma Longa) in contrast to Metformin, as well as the involvement of adiponectin in endocrine-metabolic abnormalities in experimentally induced PCOS mice model, were studied in this study. Letrozole (6 mg/kg) was administered orally (p.o) for 21 days to induce PCOS, followed by a dose of Turmeric Extract (Curcuma longa) (175 mg/kg and p.o) and Metformin (150 mg/kg) for 30 days, both with normal saline water (0.9%) as the carrier. The findings revealed that LET-treated mice displayed PCOS-like characteristics, such as higher LH levels, increased body weight growth, and ovarian morphology with numerous cysts, increase in fasting blood glucose, lipid profile, plasma lipid peroxidation (MDA) and IL-6, as well as a decrease in serum Progesterone, Estrogen, FSH, SOD and GSH levels in the ovary. These changes were linked to lower levels of circulating adiponectin and were reversed when treated Turmeric extract. By altering circulating androgen-adiponectin balance, the data implies that Turmeric extract alleviates endocrine-metabolic abnormalities and inflammation-related comorbidities associated with LET-induced PCOS.

Clozapine Induced Disturbances in Hepatic Glucose Metabolism: The Potential Role of PGRMC1 Signaling.

Newly emerging evidence has implicated that progesterone receptor component 1 (PGRMC1) plays a novel role not only in the lipid disturbance induced by atypical antipsychotic drugs (AAPD) but also in the deterioration of glucose homoeostasis induced by clozapine (CLZ) treatment. The present study aimed to investigate the role of PGRMC1 signaling on hepatic gluconeogenesis and glycogenesis in male rats following CLZ treatment (20 mg/kg daily for 4 weeks). Recombinant adeno-associated viruses (AAV) were constructed for the knockdown or overexpression of hepatic PGRMC1. Meanwhile, AG205, the specific inhibitor of PGRMC1 was also used for functional validation of PGRMC1. Hepatic protein expressions were measured by western blotting. Meanwhile, plasma glucose, insulin and glucagon, HbA1c and hepatic glycogen were also determined by assay kits. Additionally, concentrations of progesterone (PROG) in plasma, liver and adrenal gland were measured by a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. Our study demonstrated that CLZ promoted the process of gluconeogenesis and repressed glycogenesis, respectively mediated by PI3K-Akt-FOXO1 and GSK3β signaling via inhibition of PGRMC1-EGFR/GLP1R in rat liver, along with an increase in fasting blood glucose, HbA1c levels and a decrease in insulin and hepatic glycogen levels. Furthermore, through PGRMC1-EGFR/GLP1R-PI3K-Akt pathway, knockdown or inhibition (by AG205) of PGRMC1 mimics, whereas its overexpression moderately alleviates CLZ-induced glucose disturbances. Potentially, the PGRMC1 target may be regarded as a novel therapeutic strategy for AAPD-induced hepatic glucose metabolism disorder.

Midlife measures of lipid fractions and fasting glucose are associated with late‐onset Alzheimer disease

AbstractBackgroundMeasures of cardiovascular and metabolic disease are well‐established risk factors for late‐onset Alzheimer disease (AD). However, it is poorly understood whether exposure to these risk factors in early adulthood is associated with AD in late‐life.MethodAssociation of incident AD occurring after age 60 with measures of lipid fractions, hypertension, diabetes, blood glucose, BMI and smoking obtained prospectively across nine quadrennial examinations was evaluated in the Framingham Heart Study (FHS) Offspring cohort (n=5,124) using Cox proportional hazard models. Age‐ and sex‐adjusted models were tested for each risk factor measured at each exam and within three age groups (early adulthood=35‐50, middle adulthood=51‐60, late adulthood=61‐70). Additional models included covariates for risk factor‐specific treatment and APOE ε4 carrier status.ResultDuring a mean follow‐up period of 31.7±6.7 years, a diagnosis of incident AD was established for 271 participants. A 15 mg/dL increase in high‐density lipoprotein cholesterol (HDL‐C) measured during early adulthood and middle adulthood was associated with a 19.1% decreased risk of AD in each group (HR=0.81 [95%CI 0.70, 0.96], P=0.011 and HR=0.81 [0.67, 0.97], P=0.019, respectively). An increased risk of AD was also associated with 15 mg/dL increases of triglyceride (TG) (HR=1.05 [1.002, 1.10], P=0.023) and low‐density lipoprotein cholesterol (LDL‐C) (HR=1.06 [1.003, 1.12], P=0.041) measured in early adulthood. A 15 mg/dL increase in fasting blood glucose (FBG) measured during middle adulthood was associated with a 11.0% increased risk of AD (HR=1.11 [1.03, 1.20], P=0.0039). These findings remained significant after adjusting for treatment. Survival analysis showed that AD risk was significantly higher and occurred earlier among individuals with FBG in the pre‐diabetic (100‐126 mg/dL) and diabetic (>126 mg/dL) ranges compared to those with normal FBG (<100 mg/dL) in middle adulthood (P=0.038), but not in late adulthood.ConclusionHDL‐C, LDL‐C, TG and FBG levels measured in cognitively normal individuals between ages 35 and 60 years are significantly associated with incident AD several decades later. Our findings suggest that careful management of cholesterol and glucose levels beginning in early adulthood can lower AD risk in later life including among APOE ε4 carriers, in addition to the benefits of promoting cardiovascular and metabolic health.

NOX1 mediates metabolic heart disease in mice and is upregulated in monocytes of humans with diastolic dysfunction.

Microvascular inflammation plays an important role in the pathogenesis of diastolic dysfunction (DD) and metabolic heart disease. NOX1 is expressed in vascular and immune cells and has been implicated in the vascular pathology of metabolic disease. However, its contribution to metabolic heart disease is less understood. NOX1-deficient mice (KO) and male wild-type (WT) littermates were fed a high-fat high-sucrose diet (HFHS) and injected streptozotocin (75 mg/kg i.p.) or control diet (CTD) and sodium citrate. Despite similar weight gain and increase in fasting blood glucose and insulin, only WT-HFHS but not KO-HFHS mice developed concentric cardiac hypertrophy and elevated left ventricular filling pressure. This was associated with increased endothelial adhesion molecule expression, accumulation of Mac-2-, IL-1β-, and NLRP3-positive cells and nitrosative stress in WT-HFHS but not KO-HFHS hearts. Nox1 mRNA was solidly expressed in CD45+ immune cells isolated from healthy mouse hearts but was negligible in cardiac CD31+ endothelial cells. However, in vitro, Nox1 expression increased in response to lipopolysaccharide (LPS) in endothelial cells and contributed to LPS-induced upregulation of Icam-1. Nox1 was also upregulated in mouse bone marrow-derived macrophages in response to LPS. In peripheral monocytes from age- and sex-matched symptomatic patients with and without DD, NOX1 was significantly higher in patients with DD compared to those without DD. NOX1 mediates endothelial activation and contributes to myocardial inflammation and remodelling in metabolic disease in mice. Given its high expression in monocytes of humans with DD, NOX1 may represent a potential target to mitigate heart disease associated with DD.

Abstract 9880: Microplastics Exposure Promotes Cardiovascular Disease Risk in Mice

Microplastics (MPs), particles with a diameter less than 5 mm, have become a common and abundant environmental pollutant. Prior studies suggested exposure to MPs induces oxidative stress and inflammation. As these outcomes also underlie cardiovascular disease (CVD), we sought to determine if ingestion of MPs promotes cardiovascular disease risk. Thus we supplied male C57BL/6J mice (13-weeks old, n=10 in each group) with normal drinking water or that containing two sizes of polystyrene (PS) beads (0.5 μm, 5 μm) at two different doses (0.1 μg/ml and 1 μg/ml) for 12 weeks. At intervals throughout this feeding time course and at termination, we measured several indices of pre-clinical CVD. Compared with control mice, we observed a statistically significant increase in body weight in those mice consuming the 0.5 μm polystyrene beads at a dose of 1 μg/ml as early as 3 weeks after initiation of treatment. This statistically significant increase in mice body weight was maintained after 9-(1.85 fold increase versus control group) and 12-weeks (2.02 fold increase versus control group) of consumption. Furthermore, this increase in body weight appeared to be due to an increase in fat mass. Dual-energy X-ray absorptiometry (DEXA) scan analysis showed that the percent body fat significantly increased in PS exposure groups (control: 13.78±0.17% versus 17.24±0.93% in mice consuming 0.5 μm PS particles at a dose of, 1 μg/ml). In the same group of mice, we also observed an increase in fasting blood glucose (1.46 fold), fasting plasma insulin (2.50 fold), and HOMA-IR scores (2.18 fold) after 12 weeks exposure. Consistently, after analysis of a gene expression array, we found altered expression of some genes regulating adipogenesis and white adipose browning in collected perivascular adipose tissue samples. An analysis of the gut microbiome also identified changes consistent with an increase in adiposity. Thus, our results suggest that polystyrene exposure promotes adiposity and insulin resistance and is a heretofore unrecognized risk factor for atherosclerosis development and CVD.

Hepatorenal protective efficacy of flavonoids from Ocimum basilicum extract in diabetic albino rats: A focus on hypoglycemic, antioxidant, anti-inflammatory and anti-apoptotic activities

Plant derived phytochemical therapy is a bright candidate for treatment of diabetes and its associated complications. Ocimum baslicum is used as an anti-diabetic traditional medicine. Hence, the present study investigated the effect of Hail Ocimum extract (HOE) and its total flavonoids (HOETF) against hepatorenal damage in experimental diabetes induced by high-fat diet (HFD) and injection of streptozotocin (STZ) in rats. Diabetic animals were co-treated daily with HOE, HOETF or metformin (MET) as a standard anti-diabetic drug for four weeks. Compared to controls, HFD/STZ-treatment lead to significant increases in fasting blood glucose, insulin and HOMA-IR levels. Furthermore, diabetic rats had elevated hepatic (ALT and ALP) and kidney functions (urea and creatinine) biomarkers together with disturbed lipid profile and decreased PPAR-γ gene expression. Higher levels of hepatic and renal LPO and NO paralleled with lower levels of GSH and activities of antioxidant enzymes (SOD, CAT, GPx and GR) after HFD/STZ treatment. Additionally, noteworthy inflammatory and apoptotic responses were evident in both organs of diabetic rats as witnessed by augmented levels of TNF-α, IL-1b and Bax levels with declined levels of Bcl-2. Moreover, histological examination of hepatic, renal and pancreatic tissues validated the biochemical findings. On contrary, co-treatment of diabetic animals with HOE or HOETF could decrease glucose and insulin levels together with improvement of lipid markers and alleviation of hepatorenal dysfunction, oxidative injury, inflammatory and apoptotic events. Conclusively, HOE or HOETF could be a promising complementary therapeutic option for the management of diabetic hepatorenal complication owing to their antioxidant, anti-inflammatory; anti-apoptotic properties.

Assessment of Insulin, GLUT2 and inflammatory cytokines genes expression in pancreatic β-Cells in zebrafish (Danio rario) with overfeeding diabetes induction w/o glucose.

In recent years, zebrafish have been proposed as a model for rapid analysis of gene function and biological activity due to high genetic similarities with humans. The aim of this study was to determine the effects of overfeeding-induced diabetes w/o glucose on inflammatory cytokine as well as insulin and glucose transporter-2 genes (GLUT2) genes expression in the pancreas in zebrafish. The experiment was performed on 120 zebrafish (duplicated sample) with a specific genetic mapping (AB-Wild type). A total of 8 tanks, each containing 15 fish per 2-liter water, were used and divided into four groups: (1) Control group, (2) regular diet with glucose,3) Only Artemia overfeeding and 4) Combined Artemia with glucose. We induced T2DM zebrafish using glucose monohydrate solution in water and repeated daily Artemia feeding. In this model, fasting blood glucose increase is preceded by obesity and glucose intolerance. The experiment lasted for two months. Blood glucose and fish biometrics were measured in two steps. The expression of TNFα, IFNγ, GLUT2 and Insulin genes were quantified by a Real-Time qPCR System (Applied Biosystems, USA) using a set of specific primers. The highest mortality rate was observed in combined Artemia and glucose (p < 0.05). We showed significantly higher expression of IL-1B and TNF-α as well as inhibitory cytokines such as IFNγ genes in overfeeding induced diabetes(OID) which was highest in the combined Artemia and glucose group.(p < 0.05)The GLUT2 gene expression was higher in the pure artemia group which decreased to a lower level by adding glucose to Artemia in the diet. (p < 0.05). Also, the lowest insulin gene expression was observed in the combined group (p < 0.05). In zebrafish, diabetes induction with overfeeding and supraphysiological glucose in diet accompanied with higher expression of inflammatory cytokines genes in the pancreas as well as lower insulin and GLU2 genes. These epigenetic factors appeared to initiate pancreatic beta dysfunction alongside insulin resistance and could have a crucial role in the pathogenesis of overfeeding-induced diabetes using primitive animal models.

Renal Outcome and Health Related Quality of Life of Living Related Donors In Pediatric Kidney Transplantation

Objectives To assess the health related quality of life of living related donors after kidney transplantation and to evaluate clinical ,social and psychological condition post donation Study design This is an observational cross sectional study that included fifty living related donors of kidney transplant. All donors were assessed after at least one year of kidney donation. Data of the study was collected between April, 2019 and March, 2020. Methods The study included 50 living related donors;All donors were assessed after at least one year of kidney donation.WHOQOL-bref questionnaire (world health organization quality of life ) was used to assess quality of life of donors. Results The mean age at time of transplantation was 35.4±7.89 years. Eight cases developed hypertension after transplantation. There was no significant difference between serum creatinine before and after transplantation while there was significant decrease in glomerular filtration rate post transplantation. There was significant increase in fasting blood glucose and cholesterol in female donors compared to males.The results of the WHOQOL-bref questionnaire showed significant difference in results of psychological, social and environmental domains pre and post donation. Conclusion Proper selection of donors is very important to avoid complications post transplantation. Follow-up of donors should be maintained after donation.

All-trans retinoic acid impairs glucose-stimulated insulin secretion by activating the RXR/SREBP-1c/UCP2 pathway.

Diabetes is often associated with vitamin A disorders. All-trans retinoic acid (ATRA) is the main active constituent of vitamin A. We aimed to investigate whether ATRA influences diabetic progression and its mechanisms using both Goto-Kazizazi (GK) rats and INS-1 cells. Rat experiments demonstrated that ATRA treatment worsened diabetes symptoms, as evidenced by an increase in fasting blood glucose (FBG) levels and impairment of glucose homeostasis. Importantly, ATRA impaired glucose-stimulated insulin secretion (GSIS) and increased the expression of sterol regulatory element-binding protein 1c (SREBP-1c) and uncoupling protein 2 (UCP2) in the rat pancreas. Data from INS-1 cells also showed that ATRA upregulated SREBP-1c and UCP2 expression and impaired GSIS at 23 mM glucose. Srebp-1c or Ucp2 silencing attenuated GSIS impairment by reversing the ATRA-induced increase in UCP2 expression and decrease in ATP content. ATRA and the retinoid X receptor (RXR) agonists 9-cis RA and LG100268 induced the gene expression of Srebp-1c, which was almost completely abolished by the RXR antagonist HX531. RXRα-LBD luciferase reporter plasmid experiments also demonstrated that ATRA concentration-dependently activated RXRα, the EC50 of which was 1.37 μM, which was lower than the ATRA concentration in the pancreas of GK rats treated with a high dose of ATRA (approximately 3 μM), inferring that ATRA can upregulate Srebp-1c expression in the pancreas by activating RXR. In conclusion, ATRA impaired GSIS partly by activating the RXR/SREBP-1c/UCP2 pathway, thus worsening diabetic symptoms. The results highlight the roles of ATRA in diabetic progression and establish new strategies for diabetes treatment.

Establishment of long-term high-fat diet and low dose streptozotocin-induced experimental type-2 diabetes mellitus model of insulin resistance and evaluation of seed extracts of Syzygium cumini

Introduction: The principal mechanism responsible for reducing blood glucose is through insulin-stimulated glucose transport into skeletal muscle. The transporter protein that mediates this uptake is GLUT-4. A defect in this step is associated with reduced glucose utilization in muscle and adipose tissue, as observed in insulin-resistant type-2 diabetes mellitus (T2DM) patients. This study aimed to develop an experimental T2DM model and evaluate altered glucose transporter type 4 (GLUT-4) levels as a biomarker of insulin resistance. Antidiabetic activities of Syzygium cumini hydro-ethanolic seed extracts (SCE) were also evaluated. Methods: Adult male Wistar albino rats were fed a high-fat diet for 12 weeks and dosed intraperitoneally with streptozotocin (35 mg/kg). After treatment for 21 days, all investigations were done. The homeostasis model of assessment (HOMA) was used for the calculation of insulin resistance (HOMA-IR) and beta-cell function (HOMA-B) index. Diaphragm muscle and retroperitoneal fat were collected for real-time polymerase chain reaction (RT-PCR) studies. Results: A significant increase in fasting blood glucose, HOMA-IR, and serum lipids, and a decrease in serum insulin and HOMA-B were observed in the diabetic group, effects that reversed following pioglitazone and SCE treatment. The diabetic group showed a downregulation of GLUT-4 expression in skeletal muscle while an increase was observed in adipose tissue. Conclusion: A high-fat diet and low dose streptozotocin-induced experimental T2DM model of insulin resistance was developed to screen novel insulin sensitizers. Data generated demonstrated that altered GLUT-4 levels could be used as a biomarker of insulin resistance. Antidiabetic activity of S. cumini hydro-ethanolic seed extract was also confirmed in this study.

Hypoglycemic and antioxidative activities of ethanol seed extract of Hunteria umbellate (Hallier F.) on streptozotocin-induced diabetic rats

BackgroundDiabetes, a global cause of mortality in developing countries is a chronic disorder affecting the metabolism of macromolecules and has been attributed to the defective production and action of insulin characterized by persistent hyperglycemic properties. This global disorder harms organs of the body such as the liver, kidney and spleen. Medicinal plants such as Hunteria umbellate have been shown to possess hypoglycemic, antioxidative and anti-diabetic properties owing to the high concentration of active phytochemical constituents like flavonoids and alkaloids.The present study seeks to evaluate the hypoglycemic activities of ethanolic seed extract of Hunteria umbellate on streptozotocin-induced diabetes rats.MethodsThirty (30) female experimental rats were randomly divided into five groups with six rats per group and were administered streptozotocin (STZ) and Hunteria umbellate as follows. Group 1 served as control and was given only distilled water, group 2 rats were administered 60 mg/kg STZ; Group 3 was administered 60 mg/kg STZ and 100 mg/kg metformin; group 4 rats were administered 60 mg/kg STZ and 800 mg/kg Hunteria umbellate, group 5 rats 60 mg/kg STZ and 400 mg/kg Hunteria umbellate. The fasting blood glucose level of each rat was measured before sacrifice. Rats were then sacrificed 24 h after the last dose of treatment.ResultsThe results showed that Hunteria umbellate significantly reversed STZ-induced increase in fasting blood glucose and increase in body and organs weight of rats. Hunteria umbellate significantly reversed STZ-induced decrease in antioxidant enzyme in liver, kidney and spleen of rats. Hunteria umbellate significantly reversed STZ-induced increase in oxidative stress markers in liver, kidney and spleen of rats.ConclusionCollectively, our results provide convincing information that inhibition of oxidative stress and regulation of blood glucose level are major mechanisms through which Hunteria umbellate protects against streptozotocin-induced diabketes rats.

Effect of Coronavirus Infection on Fasting Blood Glucose, Kidney Function, and Electrolytes in COVID-19 Patients in the Zawia Region, Western Libya

Background: Coronavirus disease 19 (COVID-19) is a pandemic infectious disease caused by the novel coronavirus. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). It is an aggressive virus that spread worldwide and is a systemic disease involving multiple systems, including respiratory, cardiovascular, gastrointestinal, hematopoietic, neurological, immune, and urinogenital systems. Objectives: The present study aimed to evaluate the alteration in fasting blood glucose, serum urea, creatinine, Na+, K+, and Cl- levels among COVID-19 patients in the Zawia region, Western Libya. Materials and Methods: 416 confirmed COVID-19 patients hospitalized in the Isolation Centre located in Zawia city, Libya. From the 1st May 2020 to the 30th March 2021, were enrolled in this prospective study. Covid-19 patients were defined as positive cases after the detection of SARS-CoV-2 RNA in oro-nasopharyngeal swab samples. Demographic data were extracted from electronic medical records and patient files. Also, 30 healthy individuals without any chronic disease or respiratory symptoms were recruited for the control group. Blood samples were collected via vein puncture for estimating biochemical parameters (fasting blood glucose, serum urea, creatinine, Na+, K+, and Cl- concentrations). The statistical significance of differences between groups was evaluated with the Mann- Whitney (U test). Associations between different parameters were evaluated with the Spearman's test. Results: The results showed that coronavirus infection induced a significant increase in fasting blood glucose, serum urea, and creatinine concentrations. Infections also induced a decrease in serum sodium ion concentration, compared with healthy individuals. Seventy-six percent of corona virus-infected patients had hyperglycemia. Similarly, high levels of serum urea, creatinine, Cl-, Na+, and K+ were found in 40.9%, 39.9%, 27.9%, 8.9% and 6.5% of patients, respectively. Hyponatraemia, hypokalaemia, and hypochloremia were found in 35.5%, 13.7%, and 12.9% of patients. There were recorded a significant positive association between fasting blood glucose and serum urea, creatinine, and K+ concentration, between serum urea concentration and serum creatinine, K+, and Cl- concentrations, between serum creatinine and K+, and Cl- concentrations, and between serum Na+ and Cl- concentration, and a significant negative association between fasting blood glucose and serum Na+ and Cl- concentrations and between serum K+ and Na+ concentrations. Conclusion: It can be concluded that coronavirus infections induced increases in fasting blood glucose, serum urea, and creatinine, and a decrease in Na+ concentrations. There was a significant association between different parameters. These biochemical changes may help the clinicians to understand COVID-19 better and provide more clinical treatment options and prevent the serious complications of the disease. Thus, clinicians should pay special attention to fasting blood glucose, kidney function and electrolyte status of COVID-19 patients. Changes in fasting blood glucose, kidney function, and electrolyte levels can be a good indicator of disease progression.

Antidiabetic and Nephroprotective Effects of Polysaccharide Extract from the Seaweed Caulerpa racemosa in High Fructose-Streptozotocin Induced Diabetic Nephropathy.

BackgroundNephropathy is a frontline complication of diabetes mellitus (DM) associated with impaired redox-inflammatory networks. The study investigated the antidiabetic and nephroprotective potentials of PCR against diabetic nephropathy (DN) in rats.MethodsDN was induced in rats using a combination of a high fructose solution for 4 weeks and an intraperitoneal injection of streptozotocin (35 mg/kg). Diabetic rats were treated with PCR (100 and 400 mg/kg body weight) for 8 weeks. Serum biochemical parameters as well as renal oxidative stress parameters, proinflammatory cytokines, Western blot and histopathological analyses were evaluated.ResultsThere were significant increases in fasting blood glucose, urinary albumin, serum creatinine, blood urea nitrogen (BUN), total cholesterol (TC), triglycerides (TG), and low-density lipoproteins (LDL-C) levels in diabetic rats compared to the non-diabetic control rats. DM-induced DN prominently depressed renal superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities, whereas renal malondialdehyde (MDA) level was markedly increased. Furthermore, renal inflammatory cytokines, IL-1β, IL-6, TNF-α and TGF-β, were considerably elevated compared to non-diabetic control rats. Additionally, DN rats showed a significant increase in renal fibrosis, as evidenced by increased expression of TGF-β1, collagen-1, fibronectin and alpha-smooth muscle actin (α-SMA) in the kidneys. Histopathological lesions were consistent with tubule thickening and glomerular hypertrophy. Conversely, PCR treatment exerted significant attenuation of hyperglycemia, dyslipidemia and renal oxidative stress indicators. The increased renal levels of IL-1β, IL-6, TNF-α and TGF-β were also notably reversed dose-dependently with alleviation of nephropathic histology. Furthermore, PCR reduced the expression of α-SMA, fibronectin, collagen-1 and TGF-β1 in the renal tissues.ConclusionOur results suggest that PCR displayed antidiabetic and nephroprotective effects against DN by impeding oxidative stress and inflammation. As such, PCR has potentials as a food supplement for alleviating renal dysfunction caused by diabetes.

Effect of postoperative chemotherapy on blood glucose and lipid metabolism in patients with invasive breast cancer.

Chemotherapy can lead to abnormal metabolism and affect the quality of life of patients after operation. Here we explore the effect of postoperative chemotherapy on blood glucose and lipid metabolism in patients with invasive breast cancer and thus provide evidence for the prevention and treatment of blood glucose and lipid disorders after surgery. From January 2019 to December 2020, data from 141 patients with invasive breast cancer in our hospital were retrospectively collected. The levels of fasting blood glucose and blood lipid profiles [including total cholesterol, triglyceride, high-density lipoprotein (HDL), and low-density lipoprotein (LDL)] were compared before and after chemotherapy. Meanwhile, the metabolic risk factors for abnormal blood glucose and lipid profiles were analyzed. Fasting blood glucose levels significantly increased after treatment (5.21±0.89 vs. 4.87±0.71 mmol/L, P=0.000), as did those of triglyceride (1.81±1.02 vs. 1.26±0.67 mmol/L, P=0.000), while HDL significantly decreased (1.11±0.29 vs. 1.32±0.33 mmol/L, P=0.000). There were no significant differences in the levels of total cholesterol and LDL before and after treatment (P>0.05). Multivariate logistic regression analysis showed that anthracycline-based chemotherapy was a protective factor for elevated fasting blood glucose [P=0.035, 95% CI: 0.248 (0.068-0.908)], whereas receiving >6 cycles of chemotherapy was a risk factor for elevated fasting blood glucose (P=0.026, 95% CI: 4.036 (1.178-13.825)]. Postoperative chemotherapy can lead to the elevated triglyceride and fasting blood glucose and decreased HDL in patients with breast cancer. Anthracycline-based chemotherapy is a protective factor for the increase of fasting blood glucose, and more than 6 cycles of chemotherapy is a risk factor for the increase of fasting blood glucose.

Clinical characteristics and outcomes of COVID-19 patients with diabetes mellitus in Kuwait

BackgroundCOVID-19 has a highly variable clinical presentation, ranging from asymptomatic to severe respiratory symptoms and death. Diabetes seems to be one of the main comorbidities contributing to a worse COVID-19 outcome. ObjectiveIn here we analyze the clinical characteristics and outcomes of diabetic COVID-19 patients Kuwait. MethodsIn this single-center, retrospective study of 417 consecutive COVID-19 patients, we analyze and compare disease severity, outcome, associated complications, and clinical laboratory findings between diabetic and non-diabetic COVID-19 patients. ResultsCOVID-19 patients with diabetes had more ICU admission than non-diabetic COVID-19 patients (42.4% vs. 7.7%, p < 0.001). Diabetic COVID-19 patients also recorded higher mortality in comparison to non-diabetic COVID-19 patients (34.7% vs. 3.7%, p < 0.001). Diabetic COVID-19 patients had significantly higher prevalence of comorbidities, such as hypertension. Laboratory investigations also highlighted notably higher levels of C-reactive protein in diabetic COVID019 patients and lower estimated glomerular filtration rate. They also showed a higher incidence of complications. logistic regression analysis showed that every 1 mmol/L increase in fasting blood glucose in COVID-19 patients is associated with 1.52 (95% CI: 1.34–1.72, p < 0.001) times the odds of dying from COVID-19. ConclusionDiabetes is a major contributor to worsening outcomes in COVID-19 patients. Understanding the pathophysiology underlining these findings could provide insight into better management and improved outcome of such cases.

Pancreatic Islets Accumulate Cadmium in a Rodent Model of Cadmium-Induced Hyperglycemia.

Cadmium (Cd) is an anthropogenic as well as a naturally occurring toxicant associated with prediabetes and T2DM in humans and experimental models of Cd exposure. However, relatively few studies have examined the mechanism(s) of Cd-induced hyperglycemia. The purpose of this study was to examine the role of pancreatic islets in Cd-induced hyperglycemia. Male Sprague–Dawley rats were given daily subcutaneous doses of Cd at 0.6 mg/kg over 12 weeks. There was a resulting time-dependent increase in fasting blood glucose and altered insulin release in vitro. Islets isolated from control (saline-treated) and Cd-treated animals were incubated in low (0.5 mg/mL) or high (3 mg/mL) glucose conditions. Islets from 12 week Cd-treated animals had significantly less glucose-stimulated insulin release compared to islets from saline-treated control animals. The actual Cd content of isolated islets was 5 fold higher than the whole pancreas (endocrine + exocrine) and roughly 70% of that present in the renal cortex. Interestingly, islets isolated from Cd-treated animals and incubated in high glucose conditions contained significantly less Cd and zinc than those incubated in low glucose. These results show that within whole pancreatic tissue, Cd selectively accumulates in pancreatic islets and causes altered islet function that likely contributes to dysglycemia.

Ameliorative Efficacy of the Cassia auriculata Root Against High-Fat-Diet + STZ-Induced Type-2 Diabetes in C57BL/6 Mice.

Diabetes mellitus is a major metabolic disorder worldwide. Several herbs are being tested for the management of diabetes. Cassia auriculata is one of those herbs known for its nutritional value and health benefits. However, limited scientific evidence has been shown on the elucidation of its root bioactives as well as biological activity. This study attempted to identify and characterize phenolic compounds from the potent root extract and to evaluate its antioxidant as well as antidiabetic properties in both in vitro and in vivo models. The results revealed that the total polyphenol and flavonoid contents were highest in the methanolic extract. The methanolic extract of the C. auriculata root showed the highest antioxidant and antidiabetic activities in vitro than other extracts. These biological activities may be because the extract is rich in coumaric acid and −OH groups as revealed by high-performance liquid chromatography and Fourier-transform infrared spectroscopy analyses, respectively. Further, the antidiabetic activity of the methanolic extract was studied in a diet-induced type-2 diabetes mellitus (T2DM) C57BL/6 mouse model. A significant increase in fasting blood glucose and decreased plasma insulin levels in T2DM mice confirmed the development of the diabetic condition. In addition, the T2DM mice showed oxidative stress in the plasma as well as muscle tissue and significant alterations in the plasma biochemistry, viz., lipid profile, liver, and renal function tests. However, the administration of the ethanolic extract of the C. auriculata root (150 mg/kg body weight) to T2DM mice normalized the condition comparable to that of control mice. Thus, the extract can be used as a potent antioxidant and antidiabetic agent in pharmaceutical companies.

Oral L-glutamine rescues fructose-induced poor fetal outcome by preventing placental triglyceride and uric acid accumulation in Wistar rats

BackgroundMetabolic adaptation of pregnant mothers is crucial for placental development and fetal growth/survival. However, evidence exists that indiscriminate consumption of fructose-enriched drink (FED) during pregnancy disrupts maternal-fetal metabolic tolerance with attendant adverse fetal outcomes. Glutamine supplementation (GLN) has been shown to exert a modulatory effect in metabolic disorders. Nevertheless, the effects of GLN on FED-induced poor fetal outcome, and in particular the impacts on placental uric acid/lipid accumulation are unknown. The present study was conducted to test the hypothesis that oral GLN improves fetal outcome by attenuating placental lipid accumulation and uric acid synthesis in pregnant rats exposed to FED. Materials and methodsPregnant Wistar rats (160–180 g) were randomly allotted to control, GLN, FED and FED + GLN groups (6 rats/group). The groups received vehicle by oral gavage, glutamine (1 g/kg) by oral gavage, fructose (10%; w/v) and fructose + glutamine, respectively, through gestation. ResultsData showed that FED during pregnancy caused placental inefficiency, reduced fetal growth, and caused insulin resistance with correspondent increase in fasting blood glucose and plasma insulin. FED also resulted in an increased placental triglyceride, total cholesterol and de novo uric acid synthesis by activating adenosine deaminase and xanthine oxidase activities. Moreover, FED during pregnancy led to increased lipid peroxidation, lactate production with correspondent decreased adenosine and glucose-6-phosphate dehydrogenase-dependent antioxidant defense. These alterations were abrogated by GLN supplementation. ConclusionThese findings implicate that high FED intake during pregnancy causes poor fetal outcome via defective placental uric acid/triglyceride-dependent mechanism. The findings also suggest that oral GLN improves fetal outcome by ameliorating placental defects through suppression of uric acid/triglyceride accumulation.