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Gut microbiota controls the liver, as the primary regulator of the liver, according to increased evidence; however, its role in sepsis-related liver injury in the elderly is unclear. This review investigated whether metformin could attenuate SLI by modulating gut microbiota in septic-aged rats. Importantly, FMT assay revealed that rats contaminated with metformin-treated SLI rats had less frequent liver damage and colon barrier dysfunctions than those gavaged with SLI rats' faeces. The number of Klebsiella and Escherichia_Shigella was higher in SLI rats than in sham-operated and metformin-treated SLI rats, in particular, than in sham-operated and metformin-treated SLI rats, although metformin could raise the number of Bifidobacterium, Muribaculaceae, Parabacteroides_distasonis and Alloprevitella in aged SLI rats in ta in ratsia in tia_Shigella_Shigeta in SLI rats than in t si rats than t ratsi rats, Metformin-treated SLI rats, rat ratsham-treated SLI rats, Parabactero e tae, Paraphrasedo he'sia si bacterobactero bactero bacterodes_dodes_doe bactero taeta e v. Metformin, according to our findings, could cause liver damage in septic-aged rats by restricting the gut microbiota and alleviating colon barrier dysfunction, which may be an effective treatment for SLI.
Source link: https://europepmc.org/article/MED/35191819
Metformin, a common hypoglycaemic drug, has been shown to reduce body weight in type 2 diabetes, but the precise mechanism has not been completely clear. During adipogenesis, 3T3-L1 preadipocytes were used to investigate the effects of metformin on lipid droplets' morphological and physiological changes during adipogenesis. Metformin also reverses the expression pattern of genes related to adipogenesis at the transcriptome level. In the process of adipogenesis, the present study found novel changes in metformin's transcriptome, which may reveal a new mechanism by which metformin prevents obesity progression.
Source link: https://europepmc.org/article/MED/34974794
Metformin is a non-prescription, well-tolerated oral drug that is widely used as a first-line therapy for type 2 diabetes. Metformin has been shown to have anti-inflammatory effects on knee OA, according to previous observational studies and basic studies, but clinical trials must be confirmed. This research, therefore, seeks to investigate the effect of metformin versus placebo on knee cartilage volume loss and knee pain in overweight knee OA patients by a random controlled trial lasting 24 months. Discussion If metformin has been shown to reduce knee cartilage loss and knee pain among overweight knee OA patients, it may have the potential to become a disease-modifying agent for knee OA. Metformin is a low-cost substitute, with the potential role on slowing down the societal change and easing knee OA symptoms, which could significantly reduce the disease burden globally.
Source link: https://europepmc.org/article/MED/35598008
Optimum MET adsorption onto OPAC was obtained at a contact time: 240 minutes, Initial MET concentration: 5 mg/L, Temperature: 323 K, and pH 7. OPAC removed the most MET removal using OPAC by 97. 3 percent, the highest percentage of MET removal using OPAC. The sorption model best described the sorption results with the cellular sorption capacity of 50. 99 mg/g at 323 K. Langmuir isotherm model best described the sorption results with the cellular sorption capacity of 50. 99 mg/g, according to the paper using pseudo-first-order, pseudo-second-order, Elovich, and Intraparticle diffusion kinetic models, and the results best represented the pseudo-second-order kinetic model. MET sorption onto OPAC is shown by the energy of activation, E a E a, activation, suggests a physisorption mechanism for MET absorption into OPACs. Metformin removal from aqueous solution at a higher q o value than other adsorbents reported in the literature. The highest rate of removal of metformin drug-using OPAC was 97. 3 percent.
Source link: https://europepmc.org/article/MED/35594381
We systematically reviewed the evidence from both pre-clinical and human studies for the possibility of disease-modifying metformin in osteoarthritis. Methods of study Methods Between inception and June 2021 using MeSH terms and key words to find studies assessing the relationship between metformin use and outcome measures related to osteoarthritis. Metformin's effect was determined by most studies using knee osteoarthritis models. Metformin was tested for the effect on structural outcomes; immunomodulation; pain; and molecular pathways of its effect in osteoarthritis in pre-clinical studies. Conclusions We found consistent evidence from pre-clinical and human studies to support a favourable effect of metformin on knee osteoarthritis' chondroprotection, immunomodulation, and pain reduction. These results could be confirmed by further high-quality clinical trials, as metformin may be a new therapeutic agent for osteoarthritis treatment.
Source link: https://europepmc.org/article/MED/35597372
Aims To determine the safety and effectiveness of giving type 2 diabetes mellitus patients with inadequate glucose control on metformin and dipeptidyl peptidase inhibitor therapy, as well as inadequate glucose control. Materials and methods In this phase 4, double-blind, blind, placebo controlled, non-inferiority trial, patients with T2DM insufficiently managed by metformin and DPP4 inhibitor combination therapy were randomly assigned either low-dose or standard-dose lobeglitazone, respectively. In low-dose and standard-dose lobeglitazone groups, respectively, the mean HbA1c levels were 6. 870. 54% and 6. 680. 4 percent, respectively. Mean body weight changes were noticeably higher in the standard-dose group than in the low-dose group at week 24, respectively. Conclusions: Adding low-dose lobeglitazone to metformin and DPP4 inhibitor combination resulted in a non-inferior glucose-lowering result and fewer adverse events than those with standard-dose lobeglitazone.
Source link: https://europepmc.org/article/MED/35581902
Objective This research was designed to see if chronic metformin use hinders insulin resistance and cardiorespiratory fitness with aerobic exercise in people with hyperglycemia and metabolic syndrome. However, metformin use reduced VO 2MAX gains by half. Both groups demonstrated that maxitarian fat oxidation during exercise increased in both groups. Conclusions Metformin use was associated with attenuated VO 2MAX advancements, but it did not have an effect on fasting IR decreases in aerobic exercise in people with hyperglycemia and elevated cardiovascular risk.
Source link: https://europepmc.org/article/MED/35578807
This report looked at the changes of vitamin B12 levels in pediatric patients treated with metformin therapy. At 6-month, 12-month, 24-month, and 36-month intervals, researchers investigated the effect of varying doses of metformin on the mean vitamin B12 level. The degree of metformin intake on the vitamin B12 level was also investigated. Results There was no significant decline in mean vitamin B12 levels in patients treated with metformin at 6-month, 12-month, 24-month, and 36-month intervals. Mean vitamin B12 decrease was only apparent in patients receiving a high dose of metformin with high success. In addition, out of the 151 patients monitored, just one patient developed vitamin B12 deficiency after 12 months of therapy. When patients take a high dose regularly, Metformin therapy in children does not cause vitamin B12 deficiency, according to our results; however, long-term therapy may reduce vitamin B12 levels in children.
Source link: https://europepmc.org/article/MED/35592896
Whether controlling blood glucose level and T2DM, the ROS seems to induce anti-oxidative stress response by triggering nuclear factor erythroid 2-related factor 2 and glutathione peroxidase, triggering not only the elimination of ROS but also the initiation of cellular responses such as resistance to apoptosis, metabolic shifts, cell proliferation, senescence prevention, lifespan extension, and immune T cell activation against cancers.
Source link: https://europepmc.org/article/MED/35588955
The current study was designed to determine the effect of MET in functional EH and polycystic ovary syndrome. By MET administration, EH in PCOS rats was effectively blocked. MET therapy reduced the prevalence of GLUT4 in PCOS rats, which was attenuated by MET therapy. In addition, the expression of lncRNAMEG3 and lncRNASNHG20 in PCOS rats' endometrium was greatly reduced. The MET therapy also demonstrated remarkable success in restoring the expression of lncRNAMEG3 and lncRNA SNHG20. MiR223 and miR4486 expression in PCOS rats was also elevated in the endometrium, while MET treatment reduced the expression of miR223 and miR4486 in PCOS rats. miR-223 and lncRNAMEG3/GLUT4 expression, as well as miR4486 and lncRNA/GLUT4 expression, was confirmed by a luciferase assay.
Source link: https://europepmc.org/article/MED/35552758
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