Evaluation of Antidiabetic Properties of the Leaves Extract of Ficus vallis-choudae Delile in a Model of Type 2 Diabetes Induced by High-Fat Diet and Streptozotocin

This work aimed to determine the phytochemical composition of the aqueous extract of leaves of Ficus vallis-choudae (AEFV) and to evaluate its antidiabetic properties on a model of type 2 diabetes induced by a high-fat diet (HFD) and a low dose of streptozotocin (STZ). The phytochemical analysis was carried out according to several methods using the standard of each bioactive compound. Type 2 diabetes was induced by feeding rats for 4 weeks with HFD lard followed by injection of a low dose of STZ (35 mg/kg). After induction, the rats were divided into groups and treated for 28 days with metformin (40 mg/kg) and the AEFV at doses of 110, 220, and 440 mg/kg. The results showed that the AEFV contains saponins, flavonoids, tannins, and total polyphenols. In addition, it dramatically reduced body mass, body mass index (BMI), atherogenic index (AI), coronary heart risk index (CRI), and abdominal fat and increased homeostatic model assessment of β-cell function (HOMA-β), high-density lipoprotein cholesterol (HDL-c) levels, and cardioprotective index (CI). The AEFV also lowered blood glucose levels, insulinemia, homeostatic model assessment of insulin resistance (HOMA-IR) index, and total cholesterol (TC), triglycerides (TG), low-density lipoproteins cholesterol (LDL-c), and very-low-density lipoproteins cholesterol (VLDL-c) levels. There was a decrease in alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity and in urea and serum creatinine levels following the administration of AEFV. The AEFV caused increased superoxide dismutase (SOD) and catalase (CAT) activities, reduced glutathione (GSH) levels, and decreased malondialdehyde (MDA) levels in the liver, kidneys, and heart of rats. The AEFV has hypoglycemic, antioxidant, and cardioprotective properties, thus validating its use in traditional medicine for the treatment of type 2 diabetes and its complications.

Vitamin D Deficiency Is Inversely Associated with Homeostatic Model Assessment of Insulin Resistance

The study was conducted to comprehensively assess the association of the concentration of vitamin D in the blood and insulin resistance in non-diabetic subjects. The objective was to pool the results from all observational studies from the beginning of 1980 to August 2021. PubMed, Medline and Embase were systematically searched for the observational studies. Filters were used for more focused results. A total of 2248 articles were found after raw search which were narrowed down to 32 articles by the systematic selection of related articles. Homeostatic Model Assessment of Insulin Resistance (HOMAIR) was used as the measure of insulin resistance and correlation coefficient was used as a measure of the relationship between vitamin D levels and the insulin resistance. Risk of bias tables and summary plots were built using Revman software version 5.3 while Comprehensive meta-analysis version 3 was used for the construction of forest plot. The results showed an inverse association between the status of vitamin D and insulin resistance (r = −0.217; 95% CI = −0.161 to −0.272; p = 0.000). A supplement of vitamin D can help reduce the risk of insulin resistance; however further studies, like randomized controlled trials are needed to confirm the results.

Osteoglycin across the adult lifespan

Background Osteoglycin (OGN) is a proteoglycan released from bone and muscle, which has been associated with markers of metabolic health. However, it is not clear whether the levels of circulating OGN change throughout the adult lifespan or if they are associated with clinical metabolic markers or fitness. Methods 107 individuals (46 males and 61 females) aged 21-87 years were included in the study. Serum OGN levels, aerobic capacity (VO2peak), glucose and homeostatic model assessment for insulin resistance (HOMA-IR) were assessed. T-tests were used to compare participant characteristics between sexes. Regression analyses were performed to assess the relationship between OGN and age and OGN and fitness and metabolic markers. Results OGN displayed a non-linear, weak “U-shaped” relationship with age across both sexes. Males had higher levels of OGN than females across the lifespan (β=0.23, p=0.03). Age and sex explained 16% of the variance in OGN (adjusted R 2=0.16; p<0.001). Higher OGN was associated with higher VO2peak (β=0.02, p=0.001); however, those aged <50 showed a stronger positive relationship than those aged >50. A higher OGN level was associated with a higher circulating glucose level (β=0.17, p<0.01). No association was observed between OGN and HOMA-IR. Conclusions OGN was characterized by a U-shaped curve across the lifespan, which was similar between sexes. Those with a higher aerobic capacity or higher glucose concentration had higher OGN levels. Our data suggest an association between OGN and aerobic fitness and glucose regulation. Future studies should focus on exploring the potential of OGN as a biomarker for chronic disease.

Effect of Probiotic Supplementation on Glycemic Outcomes in Patients with Abnormal Glucose Metabolism: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

<b><i>Introduction:</i></b> The effectiveness of probiotics in patients with abnormal glucose metabolism has not been clearly demonstrated. It is also unclear if outcomes are consistent across different probiotic formulations. <b><i>Methods:</i></b> A literature search was conducted using PubMed, EMBASE, and Cochrane CENTRAL database from inception through May 2020. Randomized controlled trials that evaluated the effect of probiotics on fasting blood glucose (FBG) or hemoglobin A1c (HbA1c) in patients with prediabetes, type 2 diabetes mellitus, or gestational diabetes were included. Outcomes of interest included FBG, HbA1c, fasting insulin, homeostatic model assessment of insulin resistance (HOMA-IR), homeostatic model assessment of β-cell function (HOMA-B), and quantitative insulin sensitivity check index (QUICKI). Weighted mean difference (WMD) and 95% confidence intervals (CIs) were calculated using the DerSimonian and Laird random-effects model. <b><i>Results:</i></b> 31 studies involving 1,948 participants were included in this analysis. Compared to control, probiotics had a significant favorable effect on FBG (WMD −5.77 mg/dL, 95% CI −8.48 to −3.06), HbA1c (WMD −0.32%, 95% CI −0.47 to −0.18), fasting insulin (WMD −2.95 µIU/mL, 95% CI −3.76 to −2.14), HOMA-IR (WMD −0.82, 95% CI −1.05 to −0.59), HOMA-B (WMD −14.86, 95% CI −24.57 to −5.16), and QUICKI (WMD 0.015, 95% CI 0.011–0.019). Further, probiotics were associated with favorable outcomes on all parameters at doses between 1 and 10 × 10⁹ colony-forming unit per day (<i>p</i> &#x3c; 0.004 for all) and formulations containing 2–4 strains (<i>p</i> &#x3c; 0.05 for all). <b><i>Discussion/Conclusion:</i></b> Probiotics appear to have a modest effect on glycemic parameters in patients with abnormal glucose metabolism. Due to the limited number of trials conducted in patients with prediabetes, more studies are warranted in this population.

Homeostatic model of human thermoregulation with bi-stability

All homoiothermic organisms are capable of maintaining a stable body temperature using various negative feedback mechanisms. However, current models cannot satisfactorily describe the thermal adaptation of homoiothermic living systems in a physiologically meaningful way. Previously, we introduced stress entropic load, a novel variable designed to quantify adaptation costs, i.e. the stress of the organism, using a thermodynamic approach. In this study, we use stress entropic load as a starting point for the construction of a novel dynamical model of human thermoregulation. This model exhibits bi-stable mechanisms, a physiologically plausible features which has thus far not been demonstrated using a mathematical model. This finding allows us to predict critical points at which a living system, in this case a human body, may proceed towards two stabilities, only one of which is compatible with being alive. In the future, this may allow us to quantify not only the direction but rather the extent of therapeutic intervention in critical care patients.

Effects of Subacute Exposure of Dibutyl Phthalate on the Homeostatic Model Assessment, Thyroid Function, and Redox Status in Rats

Dibutyl phthalate is an endocrine disruptor used in a wide range of industrial and agriculture applications. The present study focuses on elucidating the effect of subacute exposure (4-weeks) of DBP on insulin and its sensitivity indexes, oxidative status, thyroid function, energy metabolites, serum biochemistry, and anthropometry in rats. A total of 64 rats were divided into 4 treatment groups as mg DBP/Kg body weight per day: (a) 0 mg/Kg (control), (b) 10 mg/Kg (DBP-10), (c) 50 mg/Kg (DBP-50), and (d) 100 mg/Kg (DBP-100). The rats in each treatment ( n = 16 ) were further divided into male ( n = 8 ) and female ( n = 8 ) rats for studying treatment and gender interactions. Intraperitoneal glucose tolerance test (IPGTT) was performed on the 21st day. Anthropometry, nutritional determinants, fasting plasma glucose, fasting plasma insulin, homeostatic model assessment (HOMA), thyroid hormones, energy metabolites, and oxidative status were studied during the experimental period. Two-way ANOVA was used to analyze the data ( p < 0.05 ). Tukey’s posthoc test was used for pair-wise comparisons. DBP increased body weight gain and feed efficiency in an inverted nonmonotonic U -shaped fashion. Hyperglycemia and increased blood glucose area under the curve were observed in DBP-100 at 120 minutes in IPGTT. The HOMA also showed a linear monotonic contrast. Thyroxin decreased significantly in the DBP-100 rats, whereas malondialdehyde, nonesterified fatty acids, and beta hydroxyl butyrate were increased with the DBP treatments. In conclusion, DBP could be attributed to the development of hyperglycemia and insulin resistance in rats. Further investigations into the lipid peroxidation pathways can improve our understanding of the mechanisms involved in metabolic disruption.