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Diabetes mellitus and its complications constitute a major health problem in modern societies. The disease affects approximately 5% of the adult population in western countries. The underlying process of the metabolic disorder is a defect in insulin secretion, insulin action, or both. Weight reduction, calorie restriction and patient education remain the cornerstones of the management of type 2 diabetes. When lifestyle modification fails to maintain adequate glycaemic control, insulin or oral hypoglycemic agents are typically used to manage the disease. The currently available five classes of oral agents differ in mechanism and duration of action, the degree to which they lower blood glucose and their side-effect profile. For most of these antiglycaemic agents, there is a lack of evidence on the effects on long-term complications. Only metformin has clearly proved that it can reduce mortality in obese patients with type 2 diabetes. Human insulin reduces acute and long-term mortality in patients with CVD. Furthermore, intensive treatment either with insulin or sulfonylurea has proved that it can prevent microvascular complications in type 2 diabetes. Additional randomized controlled trails assessing hard clinical endpoints are needed to better inform patients and enable physicians to establish optimal treatment strategies.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14679886&dopt=Abstract [PubMed - in process]
Zhonghua Fu Chan Ke Za Zhi. 2003 Sep;38(9):545-8.
[Effects of metformin on gonadotropin-induced ovulation in patients with polycystic ovary syndrome]
[Article in Chinese]
Zhao JZ, Ye BL, Lin JJ, Lin WQ, Chi HH.
Department of Reproductive Medicine Center, First Affiliated Hospital of Wenzhou Medical College, Wenzhou 325000, China.
OBJECTIVE: To evaluate the effects of metformin on gonadotropin-induced ovulation in patients with polycystic ovary syndrome (PCOS). METHODS: Forty patients with PCOS (study group) and 20 women with normal weight and menstrual cycle (control group) were enrolled. Serum follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone (T), fasting glucose (FG), fasting insulin (FINS) and fasting leptin were measured before and after treatment. In the study group, 20 cases (group A) were assigned to take 500 mg of metformin three times daily for 12 weeks, if pregnancy did not occur, high purified FSH (FSH-HP) was added for one cycle; another 20 cases (group B) were induced ovulation with FSH-HP alone for one cycle. RESULTS: There were significant high FINS and leptin levels in the study group as compared with the control group [(20 +/- 16) vs (12 +/- 6) nmol/L, P < 0.05; (14 +/- 16) vs (8 +/- 4) mg/L, P < 0.05]. The obese PCOS group had markedly higher serum FINS and leptin than the non-obese PCOS group [(24 +/- 18) vs (14 +/- 8) nmol/L, P < 0.05; (20 +/- 22) vs (8 +/- 4) mg/L, P < 0.05], but serum FINS and FG were not significantly different between the non-obese PCOS and the control group (P > 0.05). After administration of metformin for 12 weeks, serum LH, T, leptin and FINS decreased significantly (P < 0.05 - 0.01), serum FSH levels and body mass index showed a slight decrease, whereas no change was found in FG. In the study group, 3 cases conceived during metformin therapy, the remaining 37 were induced ovulation with FSH-HP or FSH-HP and metformin, 7 cases obtained pregnancy. The rates of ovulation and pregnancy in group A were higher than those in group B (88% vs 70%, 24% vs 15%), but no significant difference was found. CONCLUSIONS: Metformin therapy in PCOS can decrease the FINS and leptin levels, normalize the endocrine abnormalities, resumes ovulation and pregnancy in some patients, and may improve the ovarian response to gonadotropin.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14680609&dopt=Abstract
J Biol Chem. 2003 Dec 17 [Epub ahead of print]
Metformin-stimulated mannose transport in dermal fibroblasts.
Shang J, Lehrman MA.
Pharmacology Dept., UT-Southwestern Medical Center, Dallas, TX 75390-9041.
The biguanide drug metformin stimulates AMP-activated protein kinase (AMPK), a master regulator of cellular energy metabolism, and has antihyperglycemic activity due to attenuation of gluconeogenesis in hepatocytes and 2-fold stimulation of glucose transport by skeletal muscle. Here, we identify a metformin-stimulated D-mannose transport (MSMT) activity in dermal fibroblasts. MSMT increased mannose uptake 1.8-fold and had greater affinity for mannose than basal mannose transport activity. It was attributed to robust stimulation of a transporter expressed weakly in untreated cells. MSMT was not explained by greater glucose transporter activity because metformin unexpectedly decreased transport of 2-deoxy-D-glucose and 3-O-methyl-D-glucose by fibroblasts. Effective inhibitors of MSMT retained specificity for the 3-, 4-, and 6-OH groups of the mannose ring, but not the 2-OH group. Thus, MSMT could be strongly inhibited by glucose and 2-deoxy-D-glucose even though the latter was not a good transport substrate. MSMT was significant because in the presence of 2.5 mM mannose, metformin corrected experimentally induced deficiencies in the synthesis of glucose3mannose9GlcNAc2-P-P-dolichol and N-linked glycosylation. MSMT was also identified in Congenital Disorder Of Glycosylation Types Ia and Ib fibroblasts, and metformin acted synergistically with 100 uM mannose to correct LLO synthesis and N-glycosylation in the Ia cells. In conclusion, metformin activates a novel fibroblast mannose-selective transport system. This suggests that AMPK may be a regulator of mannose metabolism, and implies a therapy for CDG-Ia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14681228&dopt=Abstract [PubMed - as supplied by publisher]
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