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laennec.univ-lyon1.fr

The aim of this study was to understand by which intrahepatic mechanism metformin (Met) may inhibit basal hepatic glucose production (HGP) in type 2 diabetes. We studied rats that were fed for 6 weeks a high-fat (HF) diet, supplemented (HF-Met) or not (HF) with Met (50 mg x kg(-1) x day(-1)). Basal HGP, assessed by 3-[(3)H]glucose tracer dilution, was lower by 20% in HF-Met rats compared with HF-rats: 41.6 +/- 0.7 vs. 52 +/- 1.5 micromol x kg(-1) x min(-1) (means +/- SE, n = 5; P < 0.01). Glucose-6 phosphatase (Glc6Pase) activity, assayed in a liver lobe freeze-clamped in situ, was lower by 25% in HF-Met rats compared with HF-rats (7.9 +/- 0.4 vs. 10.3 +/- 0.9 micromol x min(-1) x g(-1) wet liver; P < 0.05). Glucose-6 phosphate and glycogen contents, e.g., 42 +/- 5 nmol/g and 3.9 +/- 2.4 mg/g, respectively, in HF-rats were dramatically increased by three to five times in HF-Met rats, e.g., 118 +/- 12 nmol/g and 19.6 +/- 4.6 mg/g (P < 0.05 and P < 0.01, respectively). Glucose-6 phosphate dehydrogenase activity was increased in HF-Met compared with HF rats (1.51 +/- 0.1 vs. 1.06 +/- 0.08 micromol x min(-1) x g(-1); P < 0.01). Intrahepatic lactate concentration tended to be lower in the Met-group (-30%; NS), whereas plasma lactate concentration was higher in HF-Met rats (1.59 +/- 0.15 mmol/l) than in HF rats (1.06 +/- 0.06 mmol/l; P < 0.05). We concluded that Met decreases HGP in insulin-resistant HF-fed rats mainly by an inhibition of hepatic Glc6Pase activity, promoting glycogen sparing. Additional mechanisms might involve the diversion of glucose-6 phosphate into the pentose phosphate pathway and an inhibition of hepatic lactate uptake.

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utu.fi

The expressions of uncoupling proteins 2 and 3 (UCP2; UCP3) mRNA were studied in obese (fa/fa) Zucker rats treated with two weight gain reducing agents for three weeks. The specific beta 3-adrenoceptor agonist BRL 35135 (0.5 mg/kg/day orally) increased the expression of UCP3 mRNA by 3.8-fold (P < 0.0001; two-way ANOVA) and that of UCP1 mRNA by 2.6-fold (P = 0.014) in brown adipose tissue, but had no effect on expression of UCP3 mRNA in white fat or in the soleus muscle, or on UCP2 mRNA expression in brown or white fat. The antihyperglycemic metformin (300 mg/kg/day orally) had no effect on expressions of UCP1, UCP2 or UCP3 in any tissue studied. Concentrations of plasma insulin were significantly correlated with the levels of white fat UCP2 mRNA (in the control group: r = 0.89, P = 0.0015) and UCP3 mRNA (in the control group: r = 0.80, P = 0.009) suggesting that insulin may play a role in the control of UCP2 and UCP3 mRNA expressions in white adipose tissue.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9618309&dopt=Abstract




Am J Obstet Gynecol. 1997 Mar;176(3):527-30.
Human placental glucose uptake and transport are not altered by the oral antihyperglycemic agent metformin.

Elliott BD, Langer O, Schuessling F.

Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, 78284-7836, USA.

OBJECTIVE: Our purpose was to determine whether the biguanide oral antihyperglycemic agent metformin increases human placental uptake and transport of glucose to the fetal circulation. STUDY DESIGN: The human single-cotyledon model was used to compare transport of tritiated glucose in the maternal to fetal direction in eight human placentas between control placentas and those exposed to metformin in vitro. Transport was calculated from the serial perfusate glucose levels obtained in each 3-hour experiment, and placental uptake was determined from homogenates of the perfused cotyledon. Liquid scintillation spectrometry measured levels of both glucose and the reference substance antipyrine. Transport was compared by the Mann-Whitney U test. RESULTS: Mean maternal and fetal glucose levels were 77.5 +/- 4.9 mg/dl and 61.3 +/- 5.9 mg/dl, respectively, in the metformin group and 83.8 +/- 4.3 mg/dl and 60.4 +/- 12.4 mg/dl, respectively, in controls at 2 hours. Placental glucose uptake was 91.1 +/- 42.2 microg/gm placenta in the metformin experiments and 104.9 +/- 76.9 microg/gm placenta in controls. No difference in placental glucose uptake or transport could be demonstrated. CONCLUSION: Metformin does not affect human placental glucose uptake or transport.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9077600&dopt=Abstract












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