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Zhonghua Fu Chan Ke Za Zhi. 2003 Dec;38(12):745-8.
[Endocrine and metabolic effects of metformin in combination with compound cyproterone acetate in women with polycystic ovarian syndrome]

[Article in Chinese]

Ye BL, Yang HY, Zhao JZ, Lin JJ, Lin WQ.

Department of Reproductive Medicine, First Affiliated Hospital, Wenzhou Medical College, Wenzhou, Zhejiang Province 325000, China.

OBJECTIVE: To study the endocrinologic and metabolic effects of metformin in combination with compound cyproterone acetate (CPA) on patients with polycystic ovarian syndrome (PCOS). METHODS: A prospective study involved total 45 PCOS patients as group A and 20 non-PCOS infertility patients as control (group B). Complete baseline work-up including body mass index (BMI), waist/hip ratio (WHR), ferriman-Gallwey score (FGS), gonadotrophin, testosterone (T), sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (Ds), insulin (FI) and glucose tolerance test, were performed in all patients. Patients in group A were treated with CPA alone (group A1), metformin alone (group A2) or combination of CPA with metformin (group A3), respectively by randomization. At the end of 12-week therapy, subjects were re-evaluated and above parameters were measured. RESULTS: Women in group A had significant increases in BMI, WHR, FGS, luteinizing hormone (LH), T, FI, insulin resistance, and significantly decrease in high-density lipoprotein (HDL)-C comparing with the control group (P < 0.01). No significant difference among A1, A2 and A3 was found at baseline. LH, T, free testosterone (FT) were significant decreased from (13.9 +/- 5.9) IU/L, (2.1 +/- 0.8) nmol/L and (2.8 +/- 2.3) nmol/L respectively to (5.8 +/- 2.2) IU/L, (1.2 +/- 0.4) nmol/L and (0.8 +/- 0.5) nmol/L respectively and SHBG was significant increased from (99 +/- 42) nmol/L to (187 +/- 64) nmol/L in group A3, when compared with LH, T and FT from (13.8 +/- 7.6) IU/L, (2.2 +/- 1.1) nmol/L and (2.5 +/- 1.9) nmol/L respectively to (11.8 +/- 6.5) IU/L, (1.8 +/- 0.8) nmol/L and (1.7 +/- 1.0) nmol/L respectively and SHBG from (99 +/- 40) nmol/L to (120 +/- 51) nmol/L in group A2 (P < 0.05 approximately 0.001). HDL-C were significantly increased from (1.5 +/- 0.3) mmol/L to (1.8 +/- 0.3) mmol/L in group A3 comparing with HDL-C from (1.5 +/- 0.4) mmol/L to (1.6 +/- 0.4) mmol/L in group A1 (P < 0.001). CONCLUSIONS: The PCOS patients treated with metformin in combination with compound cyproterone acetate may be more effective in inhibiting hyperandrogen and hypersecretion of LH than metformin alone and more obvious in improving lipid profiles than CPA alone.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14728846&dopt=Abstract [PubMed - in process]




J Biol Chem. 2004 Jan 16 [Epub ahead of print]
Activation of glycogen phosphorylase with 5-aminoimidazole-4-carboxamide riboside (AICAR): assessment of glycogen as a precursor of mannosyl residues In glycoconjugates.

Shang J, Lehrman MA.

Pharmacology Dept., UT-Southwestern Medical Center, Dallas, TX 75390-9041.

Experimental evaluation of the contribution of glycogen phosphorylase (GP) to biochemical pathways is limited to methods that raise cAMP, activating the cAMP-dependent protein kinase/phosphorylase kinase/GP cascade. Such methods convert the unphosphorylated form "GPb", which catalyzes glycogenolysis only in the presence of appropriate allosteric activators such as AMP, to the phosphorylated, constitutively activated form "GPa". However, activation of GP in this way is indirect, requires a functional cAMP kinase cascade, and is complicated by other actions of cAMP. Here, we demonstrate a strategy for experimental manipulation of GP in intact dermal fibroblasts, involving activation by the membrane-permeable adenosine analog AICAR and inhibition by caffeine and Pfizer compound CP-91149, which bind to GP at distinct sites. Potential complications due to activation of AMP-activated protein kinase by AICAR were assessed with metformin, which activates this kinase but does not activate GP. Using this strategy, we show that glycogen can be a significant and regulatable precursor of mannosyl units in lipid-linked oligosaccharides and glycoproteins.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14729664&dopt=Abstract [PubMed - as supplied by publisher]




Diabetologia. 2004 Jan 17 [Epub ahead of print]
Effects of insulin-sensitising agents in mice with hepatic insulin resistance.

Cohen SE, Tseng YH, Michael MD, Kahn CR.

Joslin Diabetes Center and Harvard Medical School, One Joslin Place, MA 02215, Boston, USA.

AIMS/HYPOTHESIS. The metabolic abnormalities of insulin resistance are ameliorated by insulin sensitisers via different mechanisms. Metformin decreases hepatic glucose output, whereas rosiglitazone (RSG) is an agonist for peroxisome proliferator activated receptor (PPAR)gamma, highly expressed in fat. To gain insight into the mechanisms of action of these drugs, we compared their actions in two models of insulin resistance: the obese, hyperglycaemic ob/ob mouse and the liver specific insulin receptor knockout (LIRKO) mouse. METHODS. Control, ob/ob, and LIRKO mice were divided into three groups that received metformin (300 mg/kg body weight/day), RSG (3 mg/kg body weight/day), or placebo for 3 weeks. RESULTS. In the presence of the severe hepatic insulin resistance of the LIRKO mouse, neither metformin nor RSG had any significant effect on glucose or insulin tolerance tests. On the other hand, RSG decreased serum concentrations of total cholesterol, LDL, and HDL in LIRKO mice. Adipocyte PPARgamma gene and protein expression, and adipocyte size were all increased in LIRKO mice treated with RSG, whereas fat-cell size in control animals was decreased by RSG. CONCLUSION/INTERPRETATION. TZDs probably improve some lipid parameters of the dysmetabolic syndrome associated with diabetes mellitus even in the presence of absolute hepatic insulin resistance, but both metformin and TZDs require an operating insulin signalling system in the liver for their effects in glucose homeostasis.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14730378&dopt=Abstract [PubMed - as supplied by publisher]





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