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The present study evaluated the efficacy of switching from premixed insulin or an insulin analogue to insulin glargine plus oral antidiabetic drugs (OADs) in patients with type 2 diabetes mellitus (T2DM). The feasibility and suitability of the regimen to the patients was examined based on islet function. Patients with T2DM (n=30) treated with stable doses of premixed insulin or an insulin analogue for eight weeks were divided into two groups according to islet function. Group A had a 2 h of C peptide (2hCP)/fasting C peptide (FCP) ratio ≤3, whereas group B had a 2hCP/FCP ratio >3. Eight weeks following the switch to insulin glargine plus OADs, a significant decrease in fasting blood glucose (FBG), 2 h postprandial blood glucose (2hPBG) and glycosylated‑haemoglobin (HbA1c) were observed in the two groups, with effective rates of 75, 42.9 and 39.3%, respectively. A distinct reduction in the insulin dose was particularly evident in group B. There was a marked decrease in FBG in group A, more so than that observed in group B. By contrast, the decrease in HbA1c was more evident in group B following the switch. A larger number of patients in group B had HbA1c≤7.0%, compared with group A. No difference in the incidence of hypoglycaemia and change of body weight were observed. Following the switch to insulin glargine plus OADs, patients with T2DM demonstrated improved blood glucose control and reduced insulin dosage. The results revealed that this switch in regimen is more suitable for patients with T2DM with 2hCP/FCP>3 and that administration of insulin glargine plus OADs is more efficacious for patients with T2DM with increased FBG levels.

Insulin therapy has been shown to contribute to extended glycemia remission in newly diagnosed patients with type 2 diabetes mellitus. This study investigated the effects of insulin treatment on pancreatic lipid content, and β-cell apoptosis and proliferation in glucose-intolerant rats to explore the protective role of insulin on β-cell function. A rat glucose-intolerant model was induced by streptozotocin and a high-fat diet. Plasma and pancreatic triglycerides, free fatty acids, and insulin were measured; and pancreatic β-cell cell apoptosis and proliferation were detected by a propidium iodide cell death assay and immunofluorescence for proliferating cell nuclear antigen. Relative β-cell area was determined by immunohistochemistry for insulin, whereas insulin production in pancreas was assessed by reverse transcriptase polymerase chain reaction. Islet β-cell secreting function was assessed by the index ΔI30/ΔG30. Glucose-intolerant rats had higher pancreatic lipid content, more islet β-cell apoptosis, lower β-cell proliferation, and reduced β-cell area in pancreas when compared with controls. Insulin therapy reduced blood glucose, inhibited pancreatic lipid accumulation and islet β-cell apoptosis, and increased β-cell proliferation and β-cell area in glucose-intolerant rats. Furthermore, impaired insulin secretion and insulin production in glucose-intolerant rats were improved by insulin therapy. Insulin can preserve β-cell function by protecting islets from glucotoxicity and lipotoxicity. It can also ameliorate β-cell area by enhancing β-cell proliferation and reducing β-cell apoptosis., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Objective: To study effects of insulin treatment on intracellular lipid content in livers and insulin resistance of type 2 diabetic rats., Methods: Type 2 diabetic rats were induced by injecting streptozotocin (25 mg/kg) and fat rich food. Then according to the results of the oral glucose tolerance test (OGTT) and glucose-induced insulin secretion test (IST), the rats were divided into two groups: control group (DC) and insulin treated group (DI). Normal rats (NC) served as controls. The treatment of each group with either NPH insulin (4 approximately 6 U . kg-1. d-1), or saline continued for 4 weeks. Body weight, OGTT, IST, blood lipids, intracellular lipids in liver and liver histology were studied. The insulin sensitivity index (ISI) was applied to assess the status of insulin resistance., Results: Blood lipid and intracellular lipids in livers in the DC were higher than those in NC (t = 2.59 approximately 15.77, P < 0.05) and the ISI was lower (t = 3.16, P < 0.05), with many fatty droplets appearing in the livers. In comparison to DC, DI showed that blood lipids were decreased, but lipids in livers were markedly increased (TG, TC, FFA increased 55.7%, 19.87%, 22.2%, respectively), and fatty droplets in hepatocytes were larger, but the ISI did not change significantly., Conclusion: Insulin treatment can make blood glucose normal, increase the intracellular lipid content in the liver, and not increase the insulin resistance significantly.

Purpose: To assess the association of type 2 diabetes mellitus (T2DM) and insulin glargine treatment with bone mineral density (BMD) in Chinese people. Methods: This retrospective study included 50 subjects with T2DM: 25 received oral glucose-lowering medication (ORL group), and 25 received oral glucose-lowering medication in combination with insulin glargine injection (CGI group). Thirty non-diabetic control subjects were also included. BMD was measured at lumbar vertebrae 1– 4 (L1–L4), spine bone mineral density (sBMD) results summary (L2–L4), femoral neck and trochanter by dual-energy x-ray absorptiometry. Results: Compared with non-diabetic controls, people with T2DM had significantly lower mean BMD at L2 (1.073± 0.120 vs 0.984± 0.158), L3 (1.094± 0.129 vs 0.991± 0.163) and L4 (1.089± 0.130 vs 0.982± 0.165) (all P< 0.05), significantly lower levels of serum calcium (2.02± 0.22 vs 2.27± 0.17 mmol/L, P< 0.05), PTH (24.19± 9.71 vs 31.52± 8.96 pg/mL, P< 0.05), and higher serum phosphate levels (1.43± 0.37 vs 1.20± 0.15 mmol/L, P< 0.05). The CGI group had higher L2, L3 and L4 BMD and sBMD (L2–L4) (P< 0.05), higher serum calcium levels (2.19± 0.11 vs 1.98± 0.20 mmol/L, P< 0.05) and lower serum phosphate levels (1.28± 0.20 vs 1.58± 0.43 mmol/L, P< 0.05) versus the ORL group. BMD and serum calcium levels were associated with the application of insulin glargine. Conclusion: These results suggest that insulin glargine may affect bone metabolism in patients diagnosed with T2DM. The study has implications for the selection of hypoglycemic agents for diabetic patients at risk of osteoporosis. [ABSTRACT FROM AUTHOR]