TY - JOUR
T1 - Pioglitazone attenuates basal and postprandial insulin concentrations and blood pressure in the spontaneously hypertensive rat
AU - Grinsell, John W.
AU - Lardinois, Claude K.
AU - Swislocki, Arthur L
AU - Gonzalez, Raymond
AU - Sare, Jeffrey S.
AU - Michaels, Jason R.
AU - Starich, Gale Hansen
PY - 2000
Y1 - 2000
N2 - Subjects with hypertension are hyperinsulinemic and resistant to insulin-stimulated glucose uptake. A similar paradigm is found in the spontaneously hypertensive rat (SHR). These findings suggest the possibility that insulin resistance and hyperinsulinemia may play an important role in blood pressure regulation. Pioglitazone, a thiazolidinedione derivative, sensitizes target tissues to insulin and decreases hyperglycemia and hyperinsulinemia in various insulin-resistant animals. The purpose of this study was to assess the influence of pioglitazone administration on pre- and postprandial glucose and insulin concentrations and determine whether changes in β-cell secretion resulted in any change in blood pressure measurements. Twelve SHR were fed custom diets ad libitum, six with and six without pioglitazone (20 mg/kg chow). Fasting and postprandial glucose levels were unaltered by pioglitazone treatment. Fasting insulin concentrations were similar at week 1, but were significantly lower (P < .01) in the pioglitazone group at weeks 3 (1.89 ± 0.3 v7.94 ± 1.5 ng/mL) and 4 (4.5 ± 1.4 v9.1 ± 0.7 ng/mL), compared with the control group. Pioglitazone also significantly (P < .01) lowered postprandial insulin concentrations after an oral glucose challenge. Systolic, mean, and diastolic blood pressures were significantly lower (P < .01), 177 ± 3 v190 ± 4.7 mm Hg, 162 ± 2.1 v175 ± 5.9 mm Hg, and 156 ± 2.1 v168 ± 6.2 mm Hg, respectively, in the animals receiving pioglitazone versus the control group. Heart rate, body weight, serum cholesterol, and triglyceride levels were comparable between the two groups. In conclusion, pioglitazone significantly decreased fasting and postprandial insulin concentrations and effectively lowered blood pressure in the SHR. (C) 2000 American Journal of Hypertension, Ltd.
AB - Subjects with hypertension are hyperinsulinemic and resistant to insulin-stimulated glucose uptake. A similar paradigm is found in the spontaneously hypertensive rat (SHR). These findings suggest the possibility that insulin resistance and hyperinsulinemia may play an important role in blood pressure regulation. Pioglitazone, a thiazolidinedione derivative, sensitizes target tissues to insulin and decreases hyperglycemia and hyperinsulinemia in various insulin-resistant animals. The purpose of this study was to assess the influence of pioglitazone administration on pre- and postprandial glucose and insulin concentrations and determine whether changes in β-cell secretion resulted in any change in blood pressure measurements. Twelve SHR were fed custom diets ad libitum, six with and six without pioglitazone (20 mg/kg chow). Fasting and postprandial glucose levels were unaltered by pioglitazone treatment. Fasting insulin concentrations were similar at week 1, but were significantly lower (P < .01) in the pioglitazone group at weeks 3 (1.89 ± 0.3 v7.94 ± 1.5 ng/mL) and 4 (4.5 ± 1.4 v9.1 ± 0.7 ng/mL), compared with the control group. Pioglitazone also significantly (P < .01) lowered postprandial insulin concentrations after an oral glucose challenge. Systolic, mean, and diastolic blood pressures were significantly lower (P < .01), 177 ± 3 v190 ± 4.7 mm Hg, 162 ± 2.1 v175 ± 5.9 mm Hg, and 156 ± 2.1 v168 ± 6.2 mm Hg, respectively, in the animals receiving pioglitazone versus the control group. Heart rate, body weight, serum cholesterol, and triglyceride levels were comparable between the two groups. In conclusion, pioglitazone significantly decreased fasting and postprandial insulin concentrations and effectively lowered blood pressure in the SHR. (C) 2000 American Journal of Hypertension, Ltd.
KW - Blood pressure
KW - Insulin
KW - Pioglitazone
KW - Spontaneously hypertensive rat
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U2 - 10.1016/S0895-7061(99)00216-2
DO - 10.1016/S0895-7061(99)00216-2
M3 - Article
C2 - 10821338
AN - SCOPUS:0034075933
VL - 13
SP - 370
EP - 375
JO - American Journal of Hypertension
JF - American Journal of Hypertension
SN - 0895-7061
IS - 4 I
ER -