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Kazuoki Inoue - One of the best experts on this subject based on the ideXlab platform.

  • Bezafibrate improves insulin resistance evaluated using the Glucose Clamp Technique in patients with type 2 diabetes mellitus: a small-scale clinical study
    Diabetology & metabolic syndrome, 2014
    Co-Authors: Hideki Shiochi, Tsuyoshi Ohkura, Yohei Fujioka, Keisuke Sumi, Naoya Yamamoto, Risa Nakanishi, Kazuhiko Matsuzawa, Schoichiro Izawa, Hiroko Ohkura, Kazuoki Inoue
    Abstract:

    Background Bezafibrate is mainly used to treat hypertriglyceridemia. Studies have reported that bezafibrate also improves type 2 diabetes mellitus, but the mechanism has not been fully elucidated. We performed euglycemic hyperinsulinemic Clamps (Glucose Clamp) and meal tolerance tests (MTT) to examine the effects of bezafibrate on insulin resistance in patients with type 2 diabetes mellitus.

  • bezafibrate improves insulin resistance evaluated using the Glucose Clamp Technique in patients with type 2 diabetes mellitus a small scale clinical study
    Diabetology & Metabolic Syndrome, 2014
    Co-Authors: Hideki Shiochi, Tsuyoshi Ohkura, Yohei Fujioka, Keisuke Sumi, Naoya Yamamoto, Risa Nakanishi, Kazuhiko Matsuzawa, Schoichiro Izawa, Hiroko Ohkura, Kazuoki Inoue
    Abstract:

    Background: Bezafibrate is mainly used to treat hypertriglyceridemia. Studies have reported that bezafibrate also improves type 2 diabetes mellitus, but the mechanism has not been fully elucidated. We performed euglycemic hyperinsulinemic Clamps (Glucose Clamp) and meal tolerance tests (MTT) to examine the effects of bezafibrate on insulin resistance in patients with type 2 diabetes mellitus. Methods: Twelve Japanese patients with type 2 diabetes mellitus and dyslipidemia (mean age: 59.5 years; fasting plasma Glucose: 7.95 mmol/L; hemoglobin A1c [HbA1c]: 7.3%; body mass index: 26.5 kg/m 2 ) underwent a Glucose Clamp and MTT before and after 12 weeks of treatment with 400 mg/day bezafibrate. The Glucose infusion rate was measured during the Glucose Clamp. The patients took a test meal (460 kcal) in the MTT. Plasma Glucose and immunoreactive insulin levels were measured at 0 (fasting), 30, 60, 120, and 180 min. Serum C-peptide immunoreactivity, serum lipids, and liver function markers were also measured during the MTT. Results: Bezafibrate significantly increased the mean Glucose infusion rate from 5.78 ± 1.94 to 6.78 ± 2.52 mg/kg/min (p < 0.05). HbA1c improved from 7.30 ± 0.55% to 7.02 ± 0.52% (p < 0.05). In the MTT, fasting plasma Glucose decreased from 7.95 ± 1.15 to 6.98 ± 1.07 mmol/L (p < 0.05). The area under the plasma Glucose curve from 0 to 180 min decreased significantly from 29.48 ± 5.07 to 27.12 ± 3.98 mmol/h/L (p < 0.05), whereas immunoreactive insulin was unchanged. Furthermore, bezafibrate also significantly improved serum lipids, with decreases in triglyceride levels from 1.84 ± 0.88 to 1.14 ± 0.41 mmol/L (p < 0.05), low-density lipoprotein cholesterol levels from 3.56 ± 0.83 to 2.92 ± 0.55 mmol/L (p < 0.05), and remnant-like particle cholesterol levels decreased from 0.25 ± 0.16 to 0.14 ± 0.06 mmol/L (p < 0.05), and increases in high-density lipoprotein cholesterol levels from 1.50 ± 0.24 to 1.66 ± 0.29 mmol/L (p < 0.05). Conclusions: Bezafibrate improved Glucose intolerance and peripheral insulin resistance in these Japanese patients with type 2 diabetes mellitus and dyslipidemia. Therefore, bezafibrate could be used to treat insulin resistance in patients with type 2 diabetes mellitus and dyslipidemia.

Sverre E. Kjeldsen - One of the best experts on this subject based on the ideXlab platform.

  • Insulin sensitivity relates to other cardiovascular risk factors in young men: validation of some modifications of the hyperinsulinaemic, isoglycaemic Glucose Clamp Technique.
    Blood pressure. Supplement, 1997
    Co-Authors: Eigil Fossum, Aud Høieggen, Andreas Moan, G. Nordby, Sverre E. Kjeldsen
    Abstract:

    Reduced peripheral sensitivity to insulin-stimulated Glucose disposal, insulin resistance, is considered to be central in the metabolic cardiovascular syndrome. The hyperinsulinaemic euglycaemic Glucose Clamp Technique was introduced by DeFronzo in 1979 and is regarded as the reference method for quantifying insulin resistance in skeletal muscle tissue. Recently, we used this Technique in young men to relate insulin resistance (inverse of insulin sensitivity) to a number of established cardiovascular risk factors. The method has undergone numerous modifications since 1979 which have not been extensively validated. Therefore, we now describe the modified hyperinsulinaemic, isoglycaemic Glucose Clamp procedure performed in our laboratory and validate some of the modifications. Five young/middle-aged men were examined twice in three weeks and then re-examined after 4 years in the same way. The intrasubject day-to-day variability in insulin sensitivity was 5%. The average reduction in insulin sensitivity after 4 years was 21%. The last 60 min of the Clamp offered a better basis for calculating Glucose disposal rate (GDR) than the last 20 min. The variation in Glucose measurements during Clamp was 5%. We thus found that our modified isoglycaemic hyperinsulinaemic Glucose Clamp Technique for assessing insulin sensitivity in skeletal muscle tissue is accurate and reproducible when performed in young/middle-aged men.

  • Effect of Angiotensin II Receptor Blockade on Fibrinolysis During Acute Hyperinsulinemia in Patients With Essential Hypertension
    Hypertension (Dallas Tex. : 1979), 1996
    Co-Authors: Ingebjørg Seljeflot, Andreas Moan, Sverre E. Kjeldsen, Endre Sandvik, Harald Arnesen
    Abstract:

    Abstract We performed the present study to investigate indirectly the in vivo effects of angiotensin II on fibrinolysis and catecholamines by treatment with losartan, a selective angiotensin II type 1 receptor antagonist. The effects were evaluated in basal conditions as well as in two different models of acute hyperinsulinemia physiologically induced by oral Glucose ingestion and by a euglycemic Glucose Clamp Technique. Twenty subjects with moderate hypertension were included in a randomized, double-blind, placebo-controlled crossover study of 4-week treatment periods. Plasma levels of catecholamines, tissue plasminogen activator activity and antigen, and plasminogen activator inhibitor type 1 activity and antigen were unchanged in the basal state after 4 weeks of treatment. During both models of hyperinsulinemia, plasminogen activator inhibitor activity and antigen decreased significantly (both P P

  • Effects of losartan on insulin sensitivity in severe hypertension : connections through sympathetic nervous system activity ?
    Journal of Human Hypertension, 1995
    Co-Authors: Andreas Moan, Aud Høieggen, G. Nordby, I Eide, Sverre E. Kjeldsen
    Abstract:

    Angiotensin II (Ang II) is one of the most potent vasoconstrictors, and the first specific and orally available Ang II-receptor antagonist, losartan (MK-954, DuP-753), has now come into clinical use. The primary site of insulin resistance, as measured by the Glucose Clamp Technique, is skeletal muscle. Losartan specifically blocks Ang II-induced vasoconstriction, namely causes vasodilation, and may thus increase Glucose delivery to skeletal muscle. We used the euglycaemic hyper-insulinaemic Glucose Clamp Technique to assess insulin sensitivity (Glucose disposal rate, GDR) or insulin (I) sensitivity index (GDR/I). In 21-year-old men we found negative correlations between GDR/I and blood viscosity (r = -0.69), haematocrit (r = -0.65), fibrinogen (r = -0.50), cholesterol/HDL ratio (r = -0.45), triglycerides (r = -0.46), body mass index (r = -0.64), waist/hip ratio (r = -0.57), resting heart rate (r = -0.46) and diastolic blood pressure (DBP) (r = -0.43), and with DBP (r = -0.62) and plasma adrenaline (r = -0.36) during mental arithmetic stress. In the Losartan Severe Hypertension Study five patients with a record of DBP > or = 115 mm Hg were examined before and on losartan monotherapy for an average of 6 weeks. GDR increased 27% and plasma noradrenaline decreased 40% (P < 0.05 for both) during treatment with losartan. Calculated whole blood viscosity decreased on losartan (P = 0.04) and the changes in GDR correlated with the changes in viscosity (r = 0.89). These results suggest that losartan, possibly by a sympathicolytic effect, lowers blood viscosity, causes vasodilation, and improves insulin sensitivity in essential hypertension.

I Eide - One of the best experts on this subject based on the ideXlab platform.

  • Vagal stimulation augments maximal (penta) gastrin-stimulated acid secretion in humans.
    Acta physiologica Scandinavica, 1999
    Co-Authors: Gunnar Qvigstad, Bjørgaas M, I Eide, Arne K. Sandvik, Helge L. Waldum
    Abstract:

    Since the late sixties, the pentagastrin test has been the standard method to examine maximal gastric acid secretion in humans. However, studies on rats and dogs have shown that maximal pentagastrin-stimulated acid secretion can be augmented by concomitant cholinergic stimulation. The aim of this study was to examine whether the combined stimulation of the vagal nerves and pentagastrin infusion could increase maximal gastric acid secretion compared with pentagastrin alone. Eight healthy medical students (seven males) were included in the study. Gastric acid secretion was determined thrice in each subject. On day one, pentagastrin (6 microg kg(-1) h(-1)) was infused. On day two, insulin-induced hypoglycaemia (plasma Glucose approximately 2.3 mM during 30 min) was obtained by applying the Glucose Clamp Technique. On day three, pentagastrin infusion and insulin induced-hypoglycaemia were combined. The combination of insulin-induced hypoglycaemia and pentagastrin infusion increased peak acid output about 20% (P = 0.018) compared with pentagastrin alone. The hypoglycaemia did not cause significant release of gastrin. It is concluded that vagal stimulation of gastric acid secretion may be safely obtained by insulin-induced hypoglycaemia when applying the Glucose Clamp Technique. In addition, maximal pentagastrin-stimulated acid secretion does not represent the maximal acid secretory capacity in humans.

  • Cholinergic stimulation augments maximal (penta) gastrin-stimulated acid secretion in man
    Gastroenterology, 1998
    Co-Authors: Helge L. Waldum, Gunnar Qvigstad, I Eide, Bjørgaas M
    Abstract:

    In the vascularly perfirsed isolated rat stomach, maximal histamine stimulated acid secretion is higher than maximal gastrin stimulated, and the former may be augmented by concomitant cholinergic stimulation. The purpose of the present study was to examine whether maximal pentagastrin stimulated acid secretion may be augmented by concomitant vagal stimulation in man. Eight students (one female, seven males) gave an informed written consent to participate in the study. Each subject was studied thrice after an overnight fast, and with an interval at least of one week. On the first day maximal pentagastrin stimulated acid secretion was assessed by giving pentagastrin at a dose of 0.1 ~tg/kg/min which previously has been shown to give maximal gastrin stimulated acid secretion. On day two, acid secretion was stimulated by insulin induced hypoglycemia applying Glucose Clamp Technique establishing a blood Glucose level of around 2.1 mmol/1 for a 30 min period. On day three, gastric acid secretion was simultaneously stimulated with pentagastrin and hypoglycemia. Insulin induced hypoglycemia was more short-lived than that stimulated by pentagastrin. Therefore maximal acid output (MAO) was higher when stimulated by pentagastrin than by insulin hypoglycemia. Peak acid output (PAO) was, however, closely similar. The combined stimulation induced an increase in PAO in all subjects when compared with that stimulated by pentagastrin or hypoglycemia alone. The augmentation of pentagastrin stimulated PAO when applying hypoglycemia simultaneously was from 5 to 50% with a median value around 20%. The present study shows that insulin induced hypoglycemia to stimulate the vagal nerves and thus gastric acid secretion, is a safe procedure when utilizing the Glucose Clamp Technique. Moreover, pentagastrin stimulated acid secretion does not represent maximal gastric secretory capacity in man.

  • Effects of losartan on insulin sensitivity in severe hypertension : connections through sympathetic nervous system activity ?
    Journal of Human Hypertension, 1995
    Co-Authors: Andreas Moan, Aud Høieggen, G. Nordby, I Eide, Sverre E. Kjeldsen
    Abstract:

    Angiotensin II (Ang II) is one of the most potent vasoconstrictors, and the first specific and orally available Ang II-receptor antagonist, losartan (MK-954, DuP-753), has now come into clinical use. The primary site of insulin resistance, as measured by the Glucose Clamp Technique, is skeletal muscle. Losartan specifically blocks Ang II-induced vasoconstriction, namely causes vasodilation, and may thus increase Glucose delivery to skeletal muscle. We used the euglycaemic hyper-insulinaemic Glucose Clamp Technique to assess insulin sensitivity (Glucose disposal rate, GDR) or insulin (I) sensitivity index (GDR/I). In 21-year-old men we found negative correlations between GDR/I and blood viscosity (r = -0.69), haematocrit (r = -0.65), fibrinogen (r = -0.50), cholesterol/HDL ratio (r = -0.45), triglycerides (r = -0.46), body mass index (r = -0.64), waist/hip ratio (r = -0.57), resting heart rate (r = -0.46) and diastolic blood pressure (DBP) (r = -0.43), and with DBP (r = -0.62) and plasma adrenaline (r = -0.36) during mental arithmetic stress. In the Losartan Severe Hypertension Study five patients with a record of DBP > or = 115 mm Hg were examined before and on losartan monotherapy for an average of 6 weeks. GDR increased 27% and plasma noradrenaline decreased 40% (P < 0.05 for both) during treatment with losartan. Calculated whole blood viscosity decreased on losartan (P = 0.04) and the changes in GDR correlated with the changes in viscosity (r = 0.89). These results suggest that losartan, possibly by a sympathicolytic effect, lowers blood viscosity, causes vasodilation, and improves insulin sensitivity in essential hypertension.

G. Nordby - One of the best experts on this subject based on the ideXlab platform.

  • Insulin sensitivity relates to other cardiovascular risk factors in young men: validation of some modifications of the hyperinsulinaemic, isoglycaemic Glucose Clamp Technique.
    Blood pressure. Supplement, 1997
    Co-Authors: Eigil Fossum, Aud Høieggen, Andreas Moan, G. Nordby, Sverre E. Kjeldsen
    Abstract:

    Reduced peripheral sensitivity to insulin-stimulated Glucose disposal, insulin resistance, is considered to be central in the metabolic cardiovascular syndrome. The hyperinsulinaemic euglycaemic Glucose Clamp Technique was introduced by DeFronzo in 1979 and is regarded as the reference method for quantifying insulin resistance in skeletal muscle tissue. Recently, we used this Technique in young men to relate insulin resistance (inverse of insulin sensitivity) to a number of established cardiovascular risk factors. The method has undergone numerous modifications since 1979 which have not been extensively validated. Therefore, we now describe the modified hyperinsulinaemic, isoglycaemic Glucose Clamp procedure performed in our laboratory and validate some of the modifications. Five young/middle-aged men were examined twice in three weeks and then re-examined after 4 years in the same way. The intrasubject day-to-day variability in insulin sensitivity was 5%. The average reduction in insulin sensitivity after 4 years was 21%. The last 60 min of the Clamp offered a better basis for calculating Glucose disposal rate (GDR) than the last 20 min. The variation in Glucose measurements during Clamp was 5%. We thus found that our modified isoglycaemic hyperinsulinaemic Glucose Clamp Technique for assessing insulin sensitivity in skeletal muscle tissue is accurate and reproducible when performed in young/middle-aged men.

  • Effects of losartan on insulin sensitivity in severe hypertension : connections through sympathetic nervous system activity ?
    Journal of Human Hypertension, 1995
    Co-Authors: Andreas Moan, Aud Høieggen, G. Nordby, I Eide, Sverre E. Kjeldsen
    Abstract:

    Angiotensin II (Ang II) is one of the most potent vasoconstrictors, and the first specific and orally available Ang II-receptor antagonist, losartan (MK-954, DuP-753), has now come into clinical use. The primary site of insulin resistance, as measured by the Glucose Clamp Technique, is skeletal muscle. Losartan specifically blocks Ang II-induced vasoconstriction, namely causes vasodilation, and may thus increase Glucose delivery to skeletal muscle. We used the euglycaemic hyper-insulinaemic Glucose Clamp Technique to assess insulin sensitivity (Glucose disposal rate, GDR) or insulin (I) sensitivity index (GDR/I). In 21-year-old men we found negative correlations between GDR/I and blood viscosity (r = -0.69), haematocrit (r = -0.65), fibrinogen (r = -0.50), cholesterol/HDL ratio (r = -0.45), triglycerides (r = -0.46), body mass index (r = -0.64), waist/hip ratio (r = -0.57), resting heart rate (r = -0.46) and diastolic blood pressure (DBP) (r = -0.43), and with DBP (r = -0.62) and plasma adrenaline (r = -0.36) during mental arithmetic stress. In the Losartan Severe Hypertension Study five patients with a record of DBP > or = 115 mm Hg were examined before and on losartan monotherapy for an average of 6 weeks. GDR increased 27% and plasma noradrenaline decreased 40% (P < 0.05 for both) during treatment with losartan. Calculated whole blood viscosity decreased on losartan (P = 0.04) and the changes in GDR correlated with the changes in viscosity (r = 0.89). These results suggest that losartan, possibly by a sympathicolytic effect, lowers blood viscosity, causes vasodilation, and improves insulin sensitivity in essential hypertension.

  • Effects of losartan on insulin sensitivity in severe hypertension: connections through sympathetic nervous system activity?
    Journal of human hypertension, 1995
    Co-Authors: A Moan, G. Nordby, A Høieggen, I K Eide, S E Kjeldsen
    Abstract:

    Angiotensin II (Ang II) is one of the most potent vasoconstrictors, and the first specific and orally available Ang II-receptor antagonist, losartan (MK-954, DuP-753), has now come into clinical use. The primary site of insulin resistance, as measured by the Glucose Clamp Technique, is skeletal muscle. Losartan specifically blocks Ang II-induced vasoconstriction, namely causes vasodilation, and may thus increase Glucose delivery to skeletal muscle. We used the euglycaemic hyper-insulinaemic Glucose Clamp Technique to assess insulin sensitivity (Glucose disposal rate, GDR) or insulin (I) sensitivity index (GDR/I). In 21-year-old men we found negative correlations between GDR/I and blood viscosity (r = -0.69), haematocrit (r = -0.65), fibrinogen (r = -0.50), cholesterol/HDL ratio (r = -0.45), triglycerides (r = -0.46), body mass index (r = -0.64), waist/hip ratio (r = -0.57), resting heart rate (r = -0.46) and diastolic blood pressure (DBP) (r = -0.43), and with DBP (r = -0.62) and plasma adrenaline (r = -0.36) during mental arithmetic stress. In the Losartan Severe Hypertension Study five patients with a record of DBP > or = 115 mm Hg were examined before and on losartan monotherapy for an average of 6 weeks. GDR increased 27% and plasma noradrenaline decreased 40% (P < 0.05 for both) during treatment with losartan. Calculated whole blood viscosity decreased on losartan (P = 0.04) and the changes in GDR correlated with the changes in viscosity (r = 0.89). These results suggest that losartan, possibly by a sympathicolytic effect, lowers blood viscosity, causes vasodilation, and improves insulin sensitivity in essential hypertension.

S E Kjeldsen - One of the best experts on this subject based on the ideXlab platform.

  • Effects of losartan on insulin sensitivity in severe hypertension: connections through sympathetic nervous system activity?
    Journal of human hypertension, 1995
    Co-Authors: A Moan, G. Nordby, A Høieggen, I K Eide, S E Kjeldsen
    Abstract:

    Angiotensin II (Ang II) is one of the most potent vasoconstrictors, and the first specific and orally available Ang II-receptor antagonist, losartan (MK-954, DuP-753), has now come into clinical use. The primary site of insulin resistance, as measured by the Glucose Clamp Technique, is skeletal muscle. Losartan specifically blocks Ang II-induced vasoconstriction, namely causes vasodilation, and may thus increase Glucose delivery to skeletal muscle. We used the euglycaemic hyper-insulinaemic Glucose Clamp Technique to assess insulin sensitivity (Glucose disposal rate, GDR) or insulin (I) sensitivity index (GDR/I). In 21-year-old men we found negative correlations between GDR/I and blood viscosity (r = -0.69), haematocrit (r = -0.65), fibrinogen (r = -0.50), cholesterol/HDL ratio (r = -0.45), triglycerides (r = -0.46), body mass index (r = -0.64), waist/hip ratio (r = -0.57), resting heart rate (r = -0.46) and diastolic blood pressure (DBP) (r = -0.43), and with DBP (r = -0.62) and plasma adrenaline (r = -0.36) during mental arithmetic stress. In the Losartan Severe Hypertension Study five patients with a record of DBP > or = 115 mm Hg were examined before and on losartan monotherapy for an average of 6 weeks. GDR increased 27% and plasma noradrenaline decreased 40% (P < 0.05 for both) during treatment with losartan. Calculated whole blood viscosity decreased on losartan (P = 0.04) and the changes in GDR correlated with the changes in viscosity (r = 0.89). These results suggest that losartan, possibly by a sympathicolytic effect, lowers blood viscosity, causes vasodilation, and improves insulin sensitivity in essential hypertension.