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  • 1
    Electronic Resource
    Electronic Resource
    Angiotensin II and the endocrine pancreas: effects on islet blood flow and insulin secretion in rats (1998)
    Springer
    Diabetologia 41 (1998), S. 127-133 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Renin-angiotensin system ; ACE inhibitor ; angiotensin II ; pancreatic islets ; insulin release ; islet microcirculation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An intrinsic angiotensin system has been described in the pancreas, with angiotensin II specific receptors being present on both exocrine, endocrine and vascular cells. The aim of the present study was to evaluate the effects of angiotensin II on insulin secretion and blood flow regulation in the pancreas. Blood flows were determined with a microsphere technique. Infusion of angiotensin II induced a dose-dependent reduction in both whole pancreatic and islet blood flow, which was most pronounced in the former. Administration of enalaprilate, an inhibitor of angiotensin-converting enzyme, and saralasin, a non-selective angiotensin II receptor antagonist, preferentially increased islet blood flow. The effects of angiotensin II on insulin release were examined by measuring insulin concentrations in the effluents from isolated perfused pancreata. In these preparations, enalaprilate affected neither basal nor glucose-stimulated insulin release, whereas angiotensin II delayed the first phase of insulin release in response to glucose. The effect of angiotensin II was probably due to initial marked vasoconstriction. The retardation of insulin release could be avoided by adding angiotensin II to the perfusion medium 20 min before glucose administration, i. e. so that the vasoconstriction had disappeared when glucose-stimulation began. The present study suggests that the angiotensin-system is important in regulation of islet blood flow and points to a pivotal role of islet blood perfusion for an adequate insulin release. [Diabetologia (1998) 41: 127–133]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050880
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  • 2
    Electronic Resource
    Electronic Resource
    The sympathetic response to euglycaemic hyperinsulinaemia (1992)
    Springer
    Diabetologia 35 (1992), S. 873-879 
    Details
    ISSN: 1432-0428
    Keywords: Sympathetic nervous system ; catecholamines ; insulin ; blood pressure ; glucose metabolism ; hypertension ; insulin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sympathetic nervous system activation by insulin has been suggested as a mechanism explaining the association between insulin resistance and hypertension. We further examined the effect of insulin by direct microneurographic muscle and skin nerve sympathetic activity recordings during euglycaemic insulin clamps in healthy subjects. The mean plasma insulin level was elevated from 5.3±0.7 to 92.2±2.2 mU/l in seven subjects during a 90-min one-step clamp. In six other subjects plasma insulin was further raised from 85.7±4.0 mU/l to 747±53 mU/l between 45–90 min (two-step clamp). Four of the latter subjects received a sham clamp with NaCl infusions only on a second recording session. At the low dose of insulin muscle nerve sympathetic activity increased from a resting level of 22.7±5.0 bursts per min to 27.7±5.0 bursts per min at 15 min (p〈0.05). The increases in muscle nerve sympathetic activity were significant (p〈0.001; ANOVA) throughout insulin infusion, with a slight further increase (from 29.2±1.6 to 32.3±1.9 bursts per min) at the supraphysiological insulin concentration. During sham clamps muscle nerve sympathetic activity did not increase. Both insulin clamps induced minor, but significant, increases in forearm venous plasma noradrenaline concentrations. Skin nerve sympathetic activity (n=3) did not change during insulin infusions. Heart rate increased slightly but significantly (p〈0.005), during the insulin clamps. Blood pressure was not notably affected. In conclusion, hyperinsulinaemia was associated with increased vasoconstrictor nerve activity to skeletal muscle and with no change of sympathetic outflow to skin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399935
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  • 3
    Electronic Resource
    Electronic Resource
    Inhibition of insulin secretion, but normal peripheral insulin sensitivity, in a patient with a malignant endocrine pancreatic tumour producing high amounts of an islet amyloid polypeptide-like molecule (1993)
    Springer
    Diabetologia 36 (1993), S. 843-849 
    Details
    ISSN: 1432-0428
    Keywords: Amylin ; endocrine pancreatic tumour ; glucose tolerance ; insulin resistance ; islet amyloid polypeptide ; pancreatic islets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide or amylin is a polypeptide secreted mainly from the pancreatic beta cells together with insulin upon stimulation. High levels of islet amyloid polypeptide have also been shown to increase the peripheral insulin resistance and consequently a role for islet amyloid polypeptide in the glucose homeostasis has been suggested. We have studied the glucose homeostasis in a patient with a malignant endocrine pancreatic tumour producing large amounts of an islet amyloid polypeptide-like molecule (about 400 times the upper reference level for islet amyloid polypeptide). This patient developed insulin-requiring diabetes mellitus shortly after the tumour diagnosis. Both intravenous and oral glucose tolerance tests revealed inhibited early responses in insulin and C-peptide release, but the insulin and C-peptide response to glucagon stimulation was less affected. Aneuglycaemic insulin clamp showed normal insulin-mediated glucose disposal. In vitro experiments, where isolated rat pancreatic islets were cultured with serum from the patient, showed a moderately decreased islet glucose oxidation rate and glucose-stimulated insulin release compared to islets cultured with serum from healthy subjects. However, culture of rat islets with normal human serum supplemented with synthetic rat islet amyloid polypeptide did not affect the glucose-stimulated insulin release. In conclusion, the observed effects show that the diabetic state in this patient was associated with an impaired glucose-stimulated insulin release but not with an increased peripheral insulin resistance. Thus, the results suggest that if islet amyloid polypeptide has diabetogenic effects they are more likely to be exerted at the level of insulin secretion than at the level of peripheral insulin sensitivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400360
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  • 4
    Electronic Resource
    Electronic Resource
    Relationship between diastolic hypertension and myocardial morphology and function in elderly males with diabetes mellitus (1996)
    Springer
    Diabetologia 39 (1996), S. 1603-1606 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Non-insulin diabetes mellitus ; hypertension ; M-mode echocardiography ; heart function.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The existence of a distinct diabetic cardiomyopathy, characterized by a raised left ventricular mass, has previously been suggested. However, as diabetes mellitus is associated with both left ventricular hypertrophy and hypertension a confounding effect of raised blood pressure in diabetic patients has to be considered. In the present cross-sectional study an echocardiographical examination was performed as part of a health screening survey in 582 males, aged 70 years. After the exclusion of subjects with coronary heart disease or those on regular antihypertensive treatment, 30 normotensive subjects with diabetes were compared with 10 subjects with non-insulin-dependent diabetes (NIDDM) and a diastolic blood pressure 90 mm Hg or more and 203 normotensive control subjects with normal glucose tolerance. Both groups with NIDDM showed a significantly increased left atrial diameter (4.4 ± 0.7 vs 4.0 ± 0.5 cm, p 〈 0.05) and an increased atrial component in diastole (A-wave, p 〈 0.01) compared to the control subjects. Left ventricular mass was, however, only marginally and not significantly elevated in the diabetic subjects when compared to the healthy control subjects (133 ± 19 and 133 ± 28 vs 128 ± 25 g/m2). Only in the subjects with concomitant diabetes and a raised blood pressure was the intraventricular septum significantly enlarged (p 〈 0.05). Thus, in the present sample no distinct diabetic cardiomyopathy with an increased left ventricular mass, independent of the influence of hypertension could be detected. The myocardial alterations in these diabetic males were restricted to an increased left atrial size and an impaired diastolic function. [Diabetologia (1996) 39: 1603–1606]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050621
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  • 5
    Electronic Resource
    Electronic Resource
    Application of prazosin is associated with an increase of insulin sensitivity in obese patients with hypertension (1988)
    Springer
    Diabetologia 31 (1988), S. 415-420 
    Details
    ISSN: 1432-0428
    Keywords: Glucose tolerance ; hypertension ; insulin sensitivity ; lipids ; prazosin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this study was to determine whether insulin sensitivity measured by the euglycaemic insulin clamp technique is lower in patients with primary hypertension than in matched healthy control subjects, and whether this sensitivity was affected after 12 weeks of antihypertensive treatment with the alpha 1-adrenoceptor blocking drug prazosin. Twelve moderately obese normoglycaemic patients (four men), with hypertension not previously treated with pharmacological agents and diastolic blood pressure above 100 mm Hg, and 12 healthy matched control subjects participated. Supine blood pressure decreased 12/5 mmHg (p〈0.01) and standing blood pressure 14/9 mmHg (p=0.001) during prazosin treatment (mean dosage 5.3±1.6 mg/day (SD)). During euglycaemic insulin clamp studies the control subjects showed a higher mean glucose uptake than the untreated hypertensive patients (7.5±1.0 and 5.8±1.9 mg·kg b.w.−1·min−1, respectively, p〈0.01). During prazosin treatment there was no significant difference between the hypertensive patients and the control subjects in this respect (6.6±2.8 and 7.5±1.0, respectively, p=0.21). During prazosin treatment, however, the disappearance rate of glucose decreased during the intravenous glucose tolerance test (from 1.7±0.9 to 1.3±0.6, p〈0.02) and the area under the glucose concentration-time curve decreased by 38% (from 473±119 to 294±99, p〈0.001). The peak insulin concentration decreased from 55±35 to 46±32 mU/l (p〈0.006) and the area under the insulin concentration-time curve was suppressed by 38% (from 2368±1597 to 1479±940, p〈0.01). This study shows that treatment of moderately obese hypertensive patients with prazosin is associated with an increase of the insulin-mediated glucose disposal and a decrease of the insulin response to an intravenous glucose load.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00271585
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