Elevated Serum Glucose Levels Research Articles

Assessing the Features of Diabetic Foot Ulcers among Individuals with Type 2 Diabetes Mellitus in Thi Qar, Iraq

Background This study aimed to evaluate the characteristics of diabetic foot ulcers in individuals with type 2 diabetes mellitus (T2DM) in Iraq. Methods The study included 881 participants with T2DM and different types of foot ulcers, who attended a specialized diabetes center. Data on demographics, clinical characteristics, biochemical investigations, comorbidities, and treatment regimens were collected and analyzed. Results The majority of the cases (96.8%) were due to T2DM, with an average age of 58 years and a mean BMI of 30 kg/m2. Participants had elevated serum creatinine, blood urea, and glucose levels, with uncontrolled HbA1c levels. Comorbidities included hypertension, ischemic heart disease, diabetic neuropathy, and retinopathy. Most participants were on insulin and statins. Diabetic foot ulcers were mainly on the right foot (48%) and classified as Grade 2 in Wagner's system. Some participants had Charcot deformity or stages of amputation. Conclusions Random plasma glucose levels and diabetic retinopathy were significantly associated with the classification of foot ulcers. Further research is needed to explore additional variables related to T2DM and foot ulcers, emphasizing the importance of glucose control and retinopathy in ulcer classification.

Glucoregulatory Properties of a Protein Hydrolysate from Atlantic Salmon (Salmo salar): Preliminary Characterization and Evaluation of DPP-IV Inhibition and Direct Glucose Uptake In Vitro.

Metabolic disorders are increasingly prevalent conditions that manifest pathophysiologically along a continuum. Among reported metabolic risk factors, elevated fasting serum glucose (FSG) levels have shown the most substantial increase in risk exposure. Ultimately leading to insulin resistance (IR), this condition is associated with notable deteriorations in the prognostic outlook for major diseases, including neurodegenerative diseases, cancer risk, and mortality related to cardiovascular disease. Tackling metabolic dysfunction, with a focus on prevention, is a critically important aspect for human health. In this study, an investigation into the potential antidiabetic properties of a salmon protein hydrolysate (SPH) was conducted, focusing on its potential dipeptidyl peptidase-IV (DPP-IV) inhibition and direct glucose uptake in vitro. Characterization of the SPH utilized a bioassay-guided fractionation approach to identify potent glucoregulatory peptide fractions. Low-molecular-weight (MW) fractions prepared by membrane filtration (MWCO = 3 kDa) showed significant DPP-IV inhibition (IC50 = 1.01 ± 0.12 mg/mL) and glucose uptake in vitro (p ≤ 0.0001 at 1 mg/mL). Further fractionation of the lowest MW fractions (<3 kDa) derived from the permeate resulted in three peptide subfractions. The subfraction with the lowest molecular weight demonstrated the most significant glucose uptake activity (p ≤ 0.0001), maintaining its potency even at a dilution of 1:500 (p ≤ 0.01).

METABOLIC SYNDROME – A COMMON CONDITION IN MODERN SOCIETIES

The presence of multiple unknowns and uncertainty factors in medical research has made it extremely challenging to distinguish the preclinical phase of a chronic disease, such as the metabolic syndrome (MS), from the initial condition of health. MS is a complex and multifactorial medical condition characterized by the presence of at least three of the following conditions: high insulin levels (normal HOMA qualitative index 2), elevated serum glucose level &gt; 126 mg/dl, patients with abdominal obesity, a body mass index (BMI) ≥ 30 kg/m2 , a lipid panel showing a triglyceride level ≥ 150 mg/dl, and HDL-CO 35 mg/dl in men and 45 mg/dl in women. In all developed countries, the number of obese people diagnosed with insulin resistance (IR) has rapidly increased to &gt; 40% in recent years. This condition precedes the development of MS. The likelihood of having MS rises with advancing age. Additionally, new research has identified other influential hormones produced by adipose tissue that significantly impact metabolism, such as lipid cytokines, leptin, adiponectin, and rezistin. Researchers believe that central obesity and the chronic inflammatory process play a key role in the development of metabolic syndrome and focus on mitochondrial dysfunction, changes in the gut microbiome, and pancreatic beta cell dysfunction. The primary determinant in averting the development of MS is humanity's struggle against its own bioenergetic entropy, which may induce catabolic processes that abbreviate life expectancy while promoting negentropy until the fulfillment of the life program predetermined in the genetic code.

Experimental and hypothetical appraisal on inhibition of glucose-induced glycation of bovine serum albumin by quercetin

BackgroundThe specificity of protein functions depends on its folding ability into a functional structure. Protein folding is an essential systemic phenomenon that prevents incorrect folding which could result in harmful aggregation. This harmful aggregation of proteins causes neurodegenerative diseases and systemic amyloidosis. Experimental and theoretical approaches were used in this study to explicate the probable mechanisms of action of quercetin in inhibition of glucose-induced glycation through estimations of percentage glycated protein, inhibited induced protein aggregation, and unoxidized bovine serum albumin thiol groups and assessments of molecular interactions of quercetin with the structures of bovine serum albumin, amyloid beta-peptide (1–42) and 3D amyloid-beta (1–42) fibrils retrieved from the protein databank (http://www.rcsb.org). ResultsThe results showed quercetin inhibited the formation of glycated protein, protein aggregation, and thiol oxidation in a concentration-dependent manner where 200 μg/ml showed the highest inhibition while 50 μg/ml depicted the least inhibition in all the studied assessments. From the docking analysis, it was observed that quercetin had a significantly higher binding affinities − 8.67 ± 0.09 kcal/mol, − 5.37 ± 0.05 kcal/mol and − 5.93 ± 0.13 kcal/mol for the bovine serum albumin, amyloid beta-peptide (1–42) and 3D amyloid-beta (1–42) fibrils respectively compared to the glucose, the inducer. Quercetin and glucose interacted with amino acid residues at the BSA subdomain IIA thus providing a clue that quercetin may impose its inhibition through the binding domain. Also, it is important to mention that the phytochemicals shared a similar interaction profile as that of glucose with the amyloid-beta. ConclusionsThese findings established the beneficial effects of quercetin as a potential agent that could alleviate hyperglycaemic-initiated disorders associated with elevated serum glucose levels.

Rare Variant in Metallothionein 1E Increases the Risk of Type 2 Diabetes in a Chinese Population.

To uncover novel targets for the treatment of type 2 diabetes (T2D) by investigating rare variants with large effects in monogenic forms of the disease. We performed whole-exome sequencing in a family with diabetes. We validated the identified gene using Sanger sequencing in additional families and diabetes- and community-based cohorts. Wild-type and variant gene transgenic mouse models were used to study the gene function. Our analysis revealed a rare variant of the metallothionein 1E (MT1E) gene, p.C36Y, in a three-generation family with diabetes. This risk allele was associated with T2D or prediabetes in a community-based cohort. MT1E p.C36 carriers had higher HbA1c levels and greater BMI than those carrying the wild-type allele. Mice with forced expression of MT1E p.C36Y demonstrated increased weight gain, elevated postchallenge serum glucose and liver enzyme levels, and hepatic steatosis, similar to the phenotypes observed in human carriers of MT1E p.C36Y. In contrast, mice with forced expression of MT1E p.C36C displayed reduced weight and lower serum glucose and serum triglyceride levels. Forced expression of wild-type and variant MT1E demonstrated differential expression of genes related to lipid metabolism. Our results suggest that MT1E could be a promising target for drug development, because forced expression of MT1E p.C36C stabilized glucose metabolism and reduced body weight, whereas MT1E p.C36Y expression had the opposite effect. These findings highlight the importance of considering the impact of rare variants in the development of new T2D treatments.

The Effects of Blood Glucose Control in the Operative Spine Patient: A Systematic Review.

To our knowledge, this is the first systematic review to evaluate the available literature on the effects of perioperative serum glucose (SG) on outcomes for patients undergoing spine surgery. This review will add insight into how the perioperative management of SG affects the outcomes of patients undergoing spine surgery. Three databases were used in this review including Embase, PubMed, and Cochrane Library. The searches were from 2012 to 2022 and included the terms "spine surgery" and "glucose level" to identify studies that demonstrated a correlation between glucose level and postoperative outcomes. Pediatric studies, those that did not specify spine surgical outcomes related to glucose levels, and non-English studies were excluded. The methodological items for nonrandomized studies score was used to assess risk of bias in the included studies. This review included a total of 9 cohort studies, both prospective and retrospective, encompassing a total of 431,156 subjects. Seven of the 9 studies reported an increased overall complication rate among patients with diabetes or with higher SG levels, and 4 studies demonstrated an increased infection rate among this population. Two studies reported an association between decreased SG levels and improved neurological recovery when a deficit was present preoperatively, and 1 of the studies found that this association was statistically significant. Limitations of this review include lack of standardization regarding type of surgery, location of the spine, and level of evidence. Most of the current literature suggests that elevated SG levels in patients undergoing spine surgery likely leads to higher complication rates and may lead to increased infection rates, and this review reinforced the current evidence. Additionally, perioperative SG levels may be associated with the extent of neurological recovery after surgery, but further investigation may be warranted. This review adds to the current body of evidence regarding perioperative SG levels and its association with complications.

Low-dose atorvastatin protects skeletal muscle mitochondria in high-fat diet-fed mice with mitochondrial autophagy inhibition and fusion enhancement

Despite the great clinical benefits of statins in cardiovascular diseases, their widespread use may lead to adverse muscle reactions associated with mitochondrial dysfunction. Some studies have demonstrated that statins provide substantial improvement to skeletal muscle health in mice. Our previous study found that oral treatment with atorvastatin (Ator, 3 mg/kg) protected myocardial mitochondria in high-fat diet (HFD)-fed mice. Therefore, this study aimed to explore the influence of low-dose Ator (3 mg/kg) on mitochondria in skeletal muscle under cholesterol overload. Male C57BL/6J mice were fed a HFD for 18 weeks and orally administered Ator (3 mg/kg) during the last 12 weeks. Ator treatment had no effects on elevated serum cholesterol and glucose levels in HFD-fed mice. Serum creatine kinase levels and the cross-sectional area of muscle cells were not affected by HFD feeding or Ator treatment. Increased expression of PINK1-LC3 II (activated mitophagy), MFN2 (fusion), and PGC-1α (biogenesis) proteins was induced in the skeletal muscles of HFD-fed mice. Treatment with Ator inhibited PINK1 and LC3 II protein expression, but further promoted MFN1, MFN2, and OPA1 expression. The impairments in mitochondrial quality and morphology in HFD-fed mice were attenuated by treatment with Ator. Furthermore, Ator treatment enhanced glucose oxidation capacity and restored ATP production in the skeletal muscles of HFD-fed mice. The study reveals that low-dose Ator has a protective effect on muscle mitochondria in mice, likely through inhibiting mitophagy and enhancing mitochondrial fusion. This suggests that skeletal muscle mitochondria may be one of low-dose Ator-mediated protective targets.

Correlation of HOMA-IR and HbA1C with hematological parameters in patient with Diabetes mellitus Type II in Kirkuk city

Objective: The aim of this study was to investigate the relationship between hematological parameters and glycemic control in patients with type 2 diabetes mellitus (DM). Materials and Methods: This case-control study included 50 patients with DM and 50 healthy controls. Blood samples were collected from all participants to measure various hematological parameters and serum glucose, insulin, and HbA1c levels. Homeostatic Model Assessment-Insulin Resistance (HOMA-IR) was calculated to evaluate insulin resistance. Statistical analysis was performed to compare the results between the groups and to determine the correlation between hematological parameters and glycemic control. Results: The results showed that serum glucose, insulin, HbA1c, serum potassium, RDW, platelet count, and MID were significantly increased in the DM group compared to the control group, while MCV was significantly decreased. The correlation analysis showed that MID, platelet count, PCT count, and PDW were positively correlated with serum glucose, HbA1c, and HOMA-IR, while MCV was negatively correlated with serum glucose and HbA1c. RBC count, RDW, and PCV were positively correlated with HbA1c and HOMA-IR. Conclusions: The study found that DM type II patients had elevated serum glucose, insulin, HOMA IR, and HbA1C levels, as well as increased serum potassium and MID-range absolute count, and decreased MCV but increased RDW. Platelet count, PCT count, and PDW were positively correlated with serum glucose, HbA1C, and HOMA IR. These hematological parameters may serve as useful markers for assessing glycemic control and insulin resistance in DM type II patients.

Effectiveness of analog of Humanin in ameliorating streptozotocin-induced diabetic nephropathy in Sprague Dawley rats

Diabetes mellitus (DM) is associated with numerous complications, including nephropathy, which principally occur due to hyperglycemia-induced oxidative stress and inflammation. Humanin (HN), a novel peptide generated from mitochondria, has anti-oxidant and anti-inflammatory potential as observed in different disease models. However, role of HN in diabetic nephropathy (DN) has not yet been explored. This study aimed to evaluate biochemical and molecular aspects of the effects of HN analog, Humanin-glycine ([S14G]-humanin) on streptozotocin (STZ)-induced rat model of DN. Ninety Sprague Dawley (SD) rats were randomly segregated into three groups – A (control), B (disease control) and C (treatment). DM type-I was induced in group B and C via single intra-peritoneal dose of STZ (45 mg/Kg). Seven days following STZ injection, rats were deemed diabetic if their blood glucose level was > 250 mg/dL. Subsequently, diabetic rats in group C were injected with [S14G]-humanin intra-peritoneally (0.4 mg/Kg/day) for sixteen weeks. Biochemical analysis revealed that diabetic rats had markedly elevated levels of serum glucose, creatinine, BUN, TNF-α, and kidney tissue SOD. Whereas, significant decline was detected in serum insulin and albumin levels. All these parameters were significantly reversed in group C after administering [S14G]-humanin. Moreover, qRT-PCR analysis displayed up-regulation of pro-inflammatory (IL-18, IL-6, IL-1α, IL-1β, TNF-α) and down-regulation of anti-inflammatory cytokines (IL-10, IL-1RN, IL-4) in diabetic rats (group B). [S14G]-humanin treatment significantly reversed the expression of IL-18 and IL-1α, however, change in relative expression of IL-6, IL-1β, TNF-α and anti-inflammatory cytokines was insignificant (group C). Conclusively, the findings of this study depicted potential therapeutic role of [S14G]-humanin in pre-clinical rodent model of DN.

The Emerging Importance of Cirsimaritin in Type 2 Diabetes Treatment.

Cirsimaritin is a dimethoxy flavon that has different biological activities such as antiproliferative, antimicrobial, and antioxidant activities. This study aims to investigate the anti-diabetic effects of cirsimaritin in a high-fat diet and streptozotocin-(HFD/STZ)-induced rat model of type 2 diabetes mellitus (T2D). Rats were fed HFD, followed by a single low dose of STZ (40 mg/kg). HFD/STZ diabetic rats were treated orally with cirsimaritin (50 mg/kg) or metformin (200 mg/kg) for 10 days before terminating the experiment and collecting plasma, soleus muscle, adipose tissue, and liver for further downstream analysis. Cirsimaritin reduced the elevated levels of serum glucose in diabetic rats compared to the vehicle control group (p < 0.001). Cirsimaritin abrogated the increase in serum insulin in the treated diabetic group compared to the vehicle control rats (p < 0.01). The homeostasis model assessment of insulin resistance (HOMA-IR) was decreased in the diabetic rats treated with cirsimaritin compared to the vehicle controls. The skeletal muscle and adipose tissue protein contents of GLUT4 (p < 0.01 and p < 0.05, respectively) and pAMPK-α1 (p < 0.05) were upregulated following treatment with cirsimaritin. Cirsimaritin was able to upregulate GLUT2 and AMPK protein expression in the liver (p < 0.01, <0.05, respectively). LDL, triglyceride, and cholesterol were reduced in diabetic rats treated with cirsimaritin compared to the vehicle controls (p < 0.001). Cirsimaritin reduced MDA, and IL-6 levels (p < 0.001), increased GSH levels (p < 0.001), and reduced GSSG levels (p < 0.001) in diabetic rats compared to the vehicle control. Cirsimaritin could represent a promising therapeutic agent to treat T2D.

New-Onset Type 1 Diabetes Mellitus (T1DM) in a Pediatric Patient with Beckwith-Wiedemann Syndrome

Abstract Introduction Beckwith-Wiedemann Syndrome (BWS) is the most common overgrowth syndrome with up to 50% of infants found to have hypoglycemia which has been believed to be related to hyperinsulinemia. However, our case report highlights a patient with the unusual presentation of concurrent BWS and T1DM along with the discussion of genetic factors that may contribute to the pathogenesis. Clinical Case We present the case of a 4-year-old African American female with a past medical history of BWS, twin gestation, prematurity, omphalocele, and patent ductus arteriosus. Her BWS had been diagnosed at birth via genetic testing which found a loss of methylation on the maternal chromosome at imprinting center 2 (IC2) on chromosome 11. During her newborn period, she did not have hypoglycemia. She presented to her primary care physician with a 2.4-kilogram weight loss, new-onset headaches, polyuria, and polydipsia for three months. She also had a viral upper respiratory tract infection a month prior to presentation. Her twin sister did not have similar complaints. Her physical exam including vital signs was reassuring. With the concern for diabetes, further work-up was done which showed an elevated serum glucose level of 681 mg/dL, and hemoglobin A1C of 12.4%. She was admitted for new-onset diabetes. Further labs on admission also showed elevated transglutaminase IgG and positive glutamic acid decarboxylase 65 (GAD65) antibody (level: 444 nmol/L, normal: ≤0.02 nmol/L). Notably, no acidosis was detected in the initial investigations and, unfortunately, due to laboratory error the diabetes antibody panel was cancelled. She was started on a basal-bolus insulin regimen with the diagnosis of new-onset T1DM without ketoacidosis. BWS does not have T1DM as a known characteristic. Hypoglycemia secondary to hyperinsulinemia rather than the opposite, such as our case, is associated with BWS. Due to this, our case is rare, and we found a case report from Europe describing a similar phenomenon. Our patient had a GAD65 antibody being positive which explains having T1DM although there are no studies showing the association of BWS with a positive GAD65 antibody. Our patient also had a viral infection prior to the diagnosis of T1DM which may have triggered autoimmunity. Further, IC2 loss of methylation present in our patient regulates the expression of CDKN1C which has been previously reported to be associated with diabetes. Conclusion Further studies will be required to identify the possible case of T1DM in a patient with BWS. We plan on obtaining a diabetes antibody panel to further assess the genetics of our patient.

Impact of clinico-biochemical variations on the etiopathogenesis of cataract: a case-control study.

Purpose: Cataract is a major cause of blindness worldwide with a greater prevalence in developing countries like India. Owing to speculations about the relationship of various biochemical markers and cataract formation this case-control study was designed with the aim to know the impact of serum blood sugar, serum electrolytes and serum calcium on the etiopathogenesis of cataract in Kashmiri population. Methods: A total of 300 cases diagnosed with cataract and 360 healthy controls were taken for the study. Serum of all the cases and controls was analyzed for blood sugar and calcium using spectrometric techniques. Sodium and potassium were analyzed using Ion-Selective Electrode technology. All the investigations were done on ABBOTT c4000 fully automatic clinical chemistry analyzer. Results: Most of the patients in our study were ≥50 years of age having posterior subcapsular cataract. The mean levels of serum fasting blood sugar (mg/dL), serum sodium (mmol/L), serum potassium (mmol/L) and serum calcium (mg/dL) were 99.4 ± 7.7; 140.4 ± 2.5; 4.2 ± 0.5; and 8.9 ± 0.5, respectively, in cases compared to 107.7 ± 12.3; 142.9 ± 5.0; 3.8 ± 0.5; and 8.3 ± 1.7, respectively, in healthy controls. A significantly higher number of cataract cases had elevated serum glucose and sodium levels, low serum potassium and calcium levels compared to healthy controls. Conclusions: Hyperglycemia, hypernatremia, hypokalemia and hypocalcemia can independently increase the patients’ risk to cataracts. Corrections in these biochemical parameters may reduce cataract incidence.

New Treatment for Type 2 Diabetes Mellitus Using a Novel Bipyrazole Compound.

2',3,3,5'-Tetramethyl-4'-nitro-2'H-1,3'-bipyrazole (TMNB) is a novel bipyrazole compound with unknown therapeutic potential in diabetes mellitus. This study aims to investigate the anti-diabetic effects of TMNB in a high-fat diet and streptozotocin-(HFD/STZ)-induced rat model of type 2 diabetes mellitus (T2D). Rats were fed HFD, followed by a single low dose of STZ (40 mg/kg). HFD/STZ diabetic rats were treated orally with TMNB (10 mg/kg) or (200 mg/kg) metformin for 10 days before terminating the experiment and collecting plasma, soleus muscle, adipose tissue, and liver for further downstream analysis. TMNB reduced the elevated levels of serum glucose in diabetic rats compared to the vehicle control group (p &lt; 0.001). TMNB abrogated the increase in serum insulin in the treated diabetic group compared to the vehicle control rats (p &lt; 0.001). The homeostasis model assessment of insulin resistance (HOMA-IR) was decreased in the diabetic rats treated with TMNB compared to the vehicle controls. The skeletal muscle and adipose tissue protein contents of GLUT4 and AMPK were upregulated following treatment with TMNB (p &lt; 0.001, &lt; 0.01, respectively). TMNB was able to upregulate GLUT2 and AMPK protein expression in liver (p &lt; 0.001, &lt; 0.001, respectively). LDL, triglyceride, and cholesterol were reduced in diabetic rats treated with TMNB compared to the vehicle controls (p &lt; 0.001, 0.01, respectively). TMNB reduced MDA and IL-6 levels (p &lt; 0.001), and increased GSH level (p &lt; 0.05) in diabetic rats compared to the vehicle controls. Conclusion: TMNB ameliorates insulin resistance, oxidative stress, and inflammation in a T2D model. TMNB could represent a promising therapeutic agent to treat T2D.

Isorhamnetin Reduces Glucose Level, Inflammation, and Oxidative Stress in High-Fat Diet/Streptozotocin Diabetic Mice Model.

Background: Isorhamnetin is a flavonoid that is found in medical plants. Several studies showed that isorhamnetin has anti-inflammatory and anti-obesity effects. This study aims to investigate the anti-diabetic effects of isorhamnetin in a high-fat diet and Streptozotocin-(HFD/STZ)-induced mice model of type 2 diabetes. Materials and Methods: Mice were fed with HFD followed by two consecutive low doses of STZ (40 mg/kg). HFD/STZ diabetic mice were treated orally with isorhamnetin (10 mg/kg) or (200 mg/kg) metformin for 10 days before sacrificing the mice and collecting plasma and soleus muscle for further analysis. Results: Isorhamnetin reduced the elevated levels of serum glucose compared to the vehicle control group (p < 0.001). Isorhamnetin abrogated the increase in serum insulin in the treated diabetic group compared to the vehicle control mice (p < 0.001). The homeostasis model assessment of insulin resistance (HOMA-IR) was decreased in diabetic mice treated with isorhamnetin compared to the vehicle controls. Fasting glucose level was significantly lower in diabetic mice treated with isorhamnetin during the intraperitoneal glucose tolerance test (IPGTT) (p < 0.001). The skeletal muscle protein contents of GLUT4 and p-AMPK-α were upregulated following treatment with isorhamnetin (p > 0.01). LDL, triglyceride, and cholesterol were reduced in diabetic mice treated with isorhamnetin compared to vehicle control (p < 0.001). Isorhamnetin reduced MDA, and IL-6 levels (p < 0.001), increased GSH levels (p < 0.001), and reduced GSSG levels (p < 0.05) in diabetic mice compared to vehicle control. Conclusions: Isorhamnetin ameliorates insulin resistance, oxidative stress, and inflammation. Isorhamnetin could represent a promising therapeutic agent to treat T2D.

QLTI-05. HBA1C AND INSULIN COVERAGE FOR NEWLY DIAGNOSED HGG PATIENTS IN THE HOSPITAL

Abstract Corticosteroids are used in the management of patients with high-grade gliomas (HGG). Corticosteroids lead to elevated serum glucose levels, necessitating sliding-scale insulin. A hemoglobin A1c (HbA1c) reflects historical serum glucose levels but it’s unclear if it predicts corticosteroid-induced hyperglycemia. We retrospectively reviewed all newly diagnosed HGG patients who were admitted between Jan 2019 to July 2021 who had an HbA1c performed at the time of their diagnosis. HbA1c is classified into: normal (&amp;lt; 5.6%), elevated (5.7 – 6.4%) and diagnostic (&amp;gt; 6.5%). We identified 86 patients of whom 29 and 16 had elevated and diagnostic HbA1c, respectively. These patients were more likely to require sliding scale insulin at least twice during their hospitalization, 64% vs 13% of those with a normal HbA1c. Only 28% of patients had a history of diabetes. There was no correlation between elevated HbA1c and the likelihood of initiating post-operative therapy, surgical complications, or BMI results. When reviewing age, 39 patients were less than 65, of which 34% had at least an elevated HbA1c. Of those older than 65, 65% had at least an elevated HbA1c. Our analysis suggests there is a predictive value of HbA1c and the need for sliding-scale insulin while receiving corticosteroids in the HGG population, especially in the older population. We recommend screening all new HGG patients with an HbA1c at the time of diagnosis, regardless if they have a history of diabetes. We also recommend monitoring serum glucose less frequently with those who have a normal HbA1c. If the HbA1c is elevated or diagnostic, they should have monitored serum glucose levels with available sliding-scale insulin. If the patient is &amp;gt; 65 years of age, they should be considered a higher risk for having hyperglycemia and HbA1c should be reviewed. Further analysis is being conducted and will be reviewed at a later date.

Prevalence of Pulmonary Tuberculosis in Diabetic Patients: Epidemiology, Immunological Basis, and Its Amalgamated Management.

Tuberculosis (TB) is one of the most widespread and infectious diseases in the world, which is brought onbyMycobacterium tuberculosis (MTB). Most infection lacks traditional signs. Latent TBis the name given to this ailment. Of these latent infections, 10% become active and cause illness. Fever, night sweats, a prolonged cough with blood-containing mucus, and weight loss are common signs of active TB infection. Diabetes, on the other hand, is a group of metabolic illnesses characterized by elevated serum glucose levels. It is a chronic metabolic condition brought on by a deficiency in insulin secretion or resistance. It is of two types, that is, type 1 and type 2. Among all the cases of diabetes, the occurrence of type 2 is more common and less fatal than type 1. The prevalence of diabetes is currently increasing in low- and middle-income nations. As both diabetes and TB come under the most widespread chronic condition; therefore, their combined effect is evaluated. In recent years, the higher occurrence of TB in patients with hyperglycemia has come to light. People with elevated blood glucose levels exhibit several risk factors that make them more vulnerable to contracting TB. This review provides information on epidemiological data about the prevalence of TB in patients with hyperglycemia. In addition, this paper discusses the immunological underpinnings of TB development in patients with diabetes mellitus and how glycemic management reduces the risk of TB infection. It illustrates how the clinical signs and radiographic evidence of TB differ between people with diabetes and healthy people and mentions diabetes and TB combined management.

Elevated levels of serum glucose, triglyceride, and liver enzymes in a rat model of 7,12 dimethylbenz[a]anthracene (DMBA)-induced carcinogenesis

ABSTRACT Background: Uncontrolled cell proliferation in cancers has a high requirement of energy and biosynthetic substrates. Glucose and triglycerides are the main source of energy as well as the primary building blocks for forming cellular components of mammalian cells.Objective: This study aims to evaluate the shifting of serum glucose, triglyceride, and nitrogen wastes in the form of urea and creatinine levels; and liver enzymes levels, alanine transaminase (ALT) and aspartate aminotransferase (AST), in rat model carcinogenesis with a single dose of 7,12-dimethylbenzanthracene (DMBA) for 16 weeks observation..Methods: The experimental animals of Rattus norvegicus strain Sprague Dawley were divided into two groups, namely the control group and the DMBA-induced group. A blood chemistry examination was carried out at weeks 4, 8, 12, and 16 post-induction using a spectrophotometer. In addition, observation of breast tumor formation and histological examination of the tumor and organs, including liver, lung, intestine, and kidney, were performed to confirm cancer formation.Results: Five of the six experimental rats (83.3%) induced by DMBA experienced breast and lung cancer formation accompanied by continuous weight loss starting at week 10 after induction. Serum glucose levels increased significantly at weeks 12 and 16 after induction, while serum triglyceride, ALT, and AST levels increased significantly from week 4 after induction until the end of the experiment. Serum urea levels did not show a significant difference from the control group. Nonetheless, creatinine decreased at the last examination.Conclusion: Elevated serum glucose, triglycerides, ALT, and AST levels escorted the chemical carcinogen-induced cancer development. Studies at the clinical level are needed to prove whether abnormally elevated of these blood chemistry levels can be used to detect the presence of cancer early.Keywords:DMBA, breast cancer, lung cancer, cancer metabolism.

Biological Actions, Implications, and Cautions of Statins Therapy in COVID-19.

The Coronavirus Disease 2019 (COVID-19) showed worse prognosis and higher mortality in individuals with obesity. Dyslipidemia is a major link between obesity and COVID-19 severity. Statins as the most common lipid regulating drugs have shown favorable effects in various pathophysiological states. Importantly, accumulating observational studies have suggested that statin use is associated with reduced risk of progressing to severe illness and in-hospital death in COVID-19 patients. Possible explanations underlie these protective impacts include their abilities of reducing cholesterol, suppressing viral entry and replication, anti-inflammation and immunomodulatory effects, as well as anti-thrombosis and anti-oxidative properties. Despite these benefits, statin therapies have side effects that should be considered, such as elevated creatinine kinase, liver enzyme and serum glucose levels, which are already elevated in severe COVID-19. Concerns are also raised whether statins interfere with the efficacy of COVID-19 vaccines. Randomized controlled trials are being conducted worldwide to confirm the values of statin use for COVID-19 treatment. Generally, the results suggest no necessity to discontinue statin use, and no evidence suggesting interference between statins and COVID-19 vaccines. However, concomitant administration of statins and COVID-19 antiviral drug Paxlovid may increase statin exposure and the risk of adverse effects, because most statins are metabolized mainly through CYP3A4 which is potently inhibited by ritonavir, a major component of Paxlovid. Therefore, more clinical/preclinical studies are still warranted to understand the benefits, harms and mechanisms of statin use in the context of COVID-19.

Syzygium samarangense leaf extract exhibits distinct antidiabetic activities: Evidences from in silico and in vivo studies

The wax apple, Syzygium samarangense , is widely used in traditional medicine. We have previously described a plethora of biological activities from its leaf extract. These include antioxidant, anti-inflammatory, antiulcer, antitrypanosomal and hepatoprotective effects. Here, we explored the antidiabetic activities from the bioactive leaf extract in silico on two crucial receptors involved in the management of diabetes disease namely peroxisome proliferator activated receptor gamma (PPARɣ) and glucagon like peptide-1 (GLP-1) and in vivo against streptozotocin-induced diabetic rats. Altogether, 457 secondary metabolites belonging to 10 classes (phenolic acids (86 compounds), flavonoids (139 compounds), anthocyanins (61 compounds), alkylphenols (17 compounds), chalcone (15 compounds), stilbenes (9 compounds), lignans (29 compounds), tannins (29 compounds), tyrosols (13 compounds), and terpenes and others (59 compounds), were docked into the active site of PPARɣ and GLP-1 receptors. From the PDB codes used for each receptor, the co-crystallized ligand was extracted and docked together with a known reference ligand. This was done simultaneously with docking the extract’s compounds to serve as references for comparative purposes. Out of the docked candidates, the top 30 compounds affording the best docking scores were compiled for further inspection and they appeared to exhibit better scores than the respective co-crystallized and reference ligands, highlighting the antidiabetic potential of the tested extract. Nine compounds exhibited highly negative scores on both receptors, demonstrating their high probability of being potent antidiabetic agents through forming stable ligand-receptor complexes. These activities were also confirmed in STZ diabetic rats where the extract reduced the elevated levels of serum glucose and lipid peroxides and increased the declined serum insulin hormone level. Taking all together, S. samarangense can be a potential candidate for further investigations for the treatment of numerous health disorders including diabetes.

Acrylamide induced glucose metabolism disorder in rats involves gut microbiota dysbiosis and changed bile acids metabolism

Acrylamide (AA) is a common food contaminant that causes glucose metabolism disorders (GMD). However, the underlying mechanism remains unclear. Female Sprague Dawley (SD) rats were treated with AA via gavage for 21 days, and the glucose and insulin levels, gut microbiota, intestinal barrier, and metabolism were analyzed. The results revealed that AA elevated serum glucose levels, reduced insulin levels and caused intestinal barrier injury. The 16S amplicon sequencing and non-targeted metabolomics showed that AA induced gut microbiota dysbiosis and bile acids (BAs) metabolism disorder. Specifically, AA decreased the abundance of Lactobacillus and Bacteroides in the cecal contents, and increased the cholic acid (CA) content in feces. Meanwhile, the expression of ileum apical sodium-dependent bile acid transporter (ASBT) responsible for CA reabsorption was suppressed. Further analysis indicated that BAs sensing nuclear receptor farnesoid X receptor (FXR) gene was activated and glucagon-like peptide-1 (GLP-1) which stimulates insulin secretion was downregulated. In addition, activation of FXR increased the expression of fibroblast growth factor 15 (FGF15), which resulted in the inhibition of hepatic BAs synthesis. Overall, this study demonstrated that AA-induced GMD is associated with the gut-microbiota-CA-FXR/GLP-1 axis. These findings add new knowledge to the AA-induced GMD and provide a basis for potential AA toxicity mitigation by manipulation of the gut microbiota.