IntroductionCombination therapy with insulin and glucagon-like peptide-1 receptor agonists (GLP-1RAs) has already been proven an efficient treatment option for type 2 diabetes. This combination can effectively improve glycated hemoglobin levels, cause weight loss and reduce the dosage of insulin. In addition, it can also reduce the risk of hypoglycemia. Several randomized controlled trials have confirmed that this treatment may be just as effective for type 1 diabetes mellitus (T1DM) patients. The objective of this meta-analysis was to assess the effects and efficacy of the treatment on glycemic changes, weight loss and insulin dosage in type 1 diabetes mellitus patients.MethodsWe searched Embase, PubMed and Cochrane for randomized controlled trials (no time restrictions) that investigated combined insulin and GLP-1 treatment. The main endpoints were measurements of glycated hemoglobin and changes in the weight and the dosage of insulin.ResultsIn total, 1093 were studies identified, and 7 studies were included in our meta-analysis. GLP-1 agonist and insulin combination therapy led to greater reductions in HbA1c levels [P = 0.03; mean difference −0.21; 95% confidence intervals (CI) (−0.40, 0.02)] and weight [P < 0.05; −3.53 (−4.86, 2.19)] compared to control treatments. The combination therapy did not significantly influence the daily weight-adjusted total insulin dose [P = 0.05; −0.11 (−0.23, 0)], but it did reduce the daily weight-adjusted bolus insulin dose [P = 0.001; −0.06 (−0.1, 0.02)].ConclusionOur meta-analysis supports the use of a combined therapeutic regimen of insulin and GLP-1RAs for treating patients with T1DM. Combination therapy with GLP-1 and insulin could achieve an ideal treatment effect on glycemic control, weight loss and bolus insulin dose in patients with T1DM.
Aims/IntroductionTo evaluate the diagnostic value of microribonucleic acid (miR) as biomarkers in patients with diabetic kidney disease (DKD).Materials and MethodsA total of 230 diabetes mellitus patients and 53 healthy participants were enrolled, and the diabetes mellitus group was further divided into normoalbuminuria, microalbuminuria and large amount of albuminuria group. MiRs of serum and urine were quantificated using real‐time polymerase chain reaction. General clinical information was collected and analyzed for the risk factors. Cut‐off values of diagnosis sensitivity were determined by receiver operating characteristic curves and the Youden Index.ResultsCompared with the healthy participants, the expression of miR‐192 in serum decreased, whereas in urine it increased with the progression of DKD. The expression of both serum and urine miR‐126 increased in the diabetes mellitus group, but no significant change was obtained among the DKD groups. The area under the curve receiver operating characteristic of both serum and urine miR‐192 was higher than that of the albumin‐to‐creatinine ratio. Combined detection of urine and serum miR‐192 has a higher specificity and lower misdiagnosis rate.ConclusionsBoth serum and urinary miR‐192 could be a potential biomarker of DKD, playing a crucial role in the prevention and treatment of DKD.
Background This study aimed to understand the mechanistic role of N-methyl-D-aspartate receptor (NMDAR) in acute fibrogenesis using models of in vivo ureter obstruction and in vitro TGF-β administration. Methods Acute renal fibrosis (RF) was induced in mice by unilateral ureteral obstruction (UUO). Histological changes were observed using Masson’s trichrome staining. The expression levels of NR1, which is the functional subunit of NMDAR, and fibrotic and epithelial-to-mesenchymal transition markers were measured by immunohistochemical and Western blot analysis. HK-2 cells were incubated with TGF-β, and NMDAR antagonist MK-801 and Ca2+/calmodulin-dependent protein kinase II (CaMKII) antagonist KN-93 were administered for pathway determination. Chronic RF was introduced by sublethal ischemia–reperfusion injury in mice, and NMDAR inhibitor dextromethorphan hydrobromide (DXM) was administered orally. Results The expression of NR1 was upregulated in obstructed kidneys, while NR1 knockdown significantly reduced both interstitial volume expansion and the changes in the expression of α-smooth muscle actin, S100A4, fibronectin, COL1A1, Snail, and E-cadherin in acute RF. TGF-β1 treatment increased the elongation phenotype of HK-2 cells and the expression of membrane-located NR1 and phosphorylated CaMKII and extracellular signal–regulated kinase (ERK). MK801 and KN93 reduced CaMKII and ERK phosphorylation levels, while MK801, but not KN93, reduced the membrane NR1 signal. The levels of phosphorylated CaMKII and ERK also increased in kidneys with obstruction but were decreased by NR1 knockdown. The 4-week administration of DXM preserved renal cortex volume in kidneys with moderate ischemic–reperfusion injury. Conclusions NMDAR participates in both acute and chronic renal fibrogenesis potentially via CaMKII-induced ERK activation.
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