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  • 1
    Electronic Resource
    Electronic Resource
    Na+/H+ antiporter properties in peripheral blood lymphocytes from normotensive obese and type 2 diabetic patients do not differ significantly from controls (1992)
    Springer
    Acta diabetologica 29 (1992), S. 237-239 
    Details
    ISSN: 1432-5233
    Keywords: Arterial hypertension ; Na+/H+ antiport ; Obesity ; Peripheral blood lymphocytes ; Type 2 diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been hypothesized that some genetic factors link different conditions characterized by the presence of insulin resistance: among them, obesity, type 2 (non-insulin-dependent) diabetes mellitus and arterial hypertension. A good candidate could be the Na+/H+ exchanger, the increased activity of which is considered a genetic marker of essential hypertension. In this study we looked at whether the Na+ dependence of the Na+/H+ antiporter is modified in obese and type 2 diabetic patients, in the absence of arterial hypertension. The activity of this ion exchanger was measured in peripheral blood lymphocytes by acidifying them in Na+-free buffer and then monitoring the recovery of intracellular pH after Na+ addition. Quiescent lymphocytes were used because they do not have insulin receptors, thus ruling out the effects of the elevated insulin concentrations on the Na+/H+ exchanger activity. Antiport activity, measured as the ability to extrude H+ in the presence of external Na+, showed no differences in normotensive obese and type 2 diabetic patients when compared with healthy subjects. Our data therefore suggest that an altered Na+/H+ exchange activity cannot be considered a common feature of insulin-resistant states.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00573496
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  • 2
    Electronic Resource
    Electronic Resource
    Insulin increases cyclic nucleotide content in human vascular smooth muscle cells: a mechanism potentially involved in insulin-induced modulation of vascular tone (1995)
    Springer
    Diabetologia 38 (1995), S. 936-941 
    Details
    ISSN: 1432-0428
    Keywords: Key words Insulin ; arterial hypertension ; vasodilation ; vascular smooth muscle cells ; cyclic adenosine monophosphate ; cyclic guanosine monophosphate ; nitric oxide.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been suggested that insulin exerts a vasodilating effect, but the mechanisms involved are not completely understood. Since cyclic nucleotides mediate the vasodilation induced by endogenous substances, such as prostacyclin and nitric oxide, we aimed to investigate the influence of insulin (concentration range 240–960 pmol/l) on both cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) content in human vascular smooth muscle cells. Insulin dose-dependently increased both nucleotides (cAMP: from 0.7 ± 0.1 to 2.6 ± 0.4 pmol/106 cells, p = 0.0001; cGMP: from 1.3 ± 0.2 to 3.4 ± 0.7 pmol/106 cells, p = 0.033). This increase is receptor-mediated, since it was blunted when cells were preincubated with the tyrosine kinase inhibitor genistein. The effect of insulin remained significant (p = 0.0001) when preincubation with the phosphodiesterase inhibitor theophylline prevented cyclic nucleotide catabolism. The increase of cGMP was blunted when the cells were preincubated with the guanylate cyclase inhibitor methylene blue, and with the nitric oxide-synthase inhibitor NG-monomethyl-l-arginine. At all the concentrations tested, insulin potentiated the increase of cAMP induced by the stable prostacyclin analogue Iloprost (p = 0.0001), whereas only at 1920 pmol/l did it potentiate the cGMP increase induced by glyceryltrinitrate (p = 0.05). This study demonstrates that the vasodilating effects exerted by insulin may at least in part be attributable to an increase of both cGMP and cAMP via a receptor-mediated activation of adenylate and guanylate cyclases in human vascular smooth muscle cells and that the insulin effect on cGMP is mediated by nitric oxide. [Diabetologia (1995) 38: 936–941]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400582
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  • 3
    Electronic Resource
    Electronic Resource
    Insulin, insulin resistance and platelet function: similarities with insulin effects on cultured vascular smooth muscle cells (1998)
    Springer
    Diabetologia 41 (1998), S. 609-622 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin ; Insulin resistance ; Platelets ; Vascular Smooth Muscle ; Calcium ; cGMP ; cAMP ; Nitric oxide ; Prostacyclin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050958
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  • 4
    Electronic Resource
    Electronic Resource
    Insulin-induced hypoglycaemia increases plasma concentrations of angiotensin II and does not modify atrial natriuretic polypeptide secretion in man (1988)
    Springer
    Diabetologia 31 (1988), S. 816-820 
    Details
    ISSN: 1432-0428
    Keywords: Hypoglycaemia ; plasma renin activity ; angiotensin II ; aldosterone ; alpha-human atrial natriuretic polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin-induced hypoglycaemia causes profound haemodynamic changes, commonly ascribed to catecholamine increase. The aim of the present study was to investigate the influence of insulin-induced hypoglycaemia on nonadrenergic factors potentially involved in haemodynamic regulation: angiotensin II and alpha-human atrial natriuretic polypeptide. Fourteen healthy male subjects, aged 25.5±0.74 years, body mass index 23.81±0.68 kg/m2, received (after an overnight fast and at least 60 min rest in a supine position) an i.v. bolus injection of human regular insulin (Actrapid HM, Novo, Bagsvaerd, Denmark: 3.84 U/m2). Serial venous blood samples were drawn in the following 150 min, to measure plasma glucose, angiotensin II, alpha-human natriuretic polypeptide, and factors potentially involved in the regulation of the renin-angiotensin-aldosterone system. During the study, we observed a plasma glucose fall, reaching a nadir of 1.95±0.11 mmol/l between 25 and 30 min, and an increase of angiotensin II (from 7.6±0.8 to 13.5±1.1 pg/ml, p = 0.01, quadratic model evaluated by an analysis of the variance for repeated measures), whereas atrial natriuretic polypeptide remained unchanged. As far as the regulation of the renin-arigiotensin-aldosterone system is concerned, the increase of angiotensin II is attributable to the increased plasma renin activity, whereas angiotensin converting enzyme was not modified. The increase of plasma renin activity, in turn, is attributable both to the increased catecholamine concentrations and to the decreased potassium levels. Both adrenocorticotropic hormone and angiotensin II are potentially involved in the hypoglycaemia-induced increase of aldosterone concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00277483
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  • 5
    Electronic Resource
    Electronic Resource
    Human vascular smooth muscle cells express a constitutive nitric oxide synthase that insulin rapidly activates, thus increasing guanosine 3′ : 5′-cyclic monophosphate and adenosine 3′ : 5′-cyclic monophosphate concentrations (1999)
    Springer
    Diabetologia 42 (1999), S. 831-839 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin ; nitric oxide ; constitutive nitric oxide synthase ; vascular smooth muscle ; adenosine 3′ : 5′-cyclic monophosphate ; guanosine 3′ : 5′-cyclic monophosphate.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Insulin incubation of human vascular smooth muscle cells (hVSMC) for 120 min increases both guanosine 3′ : 5′-cyclic monophosphate (cGMP) and adenosine 3′ : 5′-cyclic monophosphate (cAMP) and these effects are blocked by inhibiting nitric oxide synthase (NOS). These data suggest that insulin activates a constitutive Ca2+-dependent NOS (cNOS), not described at yet in hVSMC. To test this hypothesis, we evaluated in hVSMC: i) the kinetics of the insulin-induced enhancement of the two cyclic nucleotides; ii) the ability of nitric oxide (NO) to increase both cyclic nucleotides; iii) NO involvement in the short-term influence of insulin on both cyclic nucleotides; iv) the ability of insulin to increase NO production in a few minutes; v) the presence of a cNOS activity; vi) the expression of mRNA for cNOS. Methods. In hVSMC incubated with insulin, NO donors and the Ca2+ ionophore ionomycin, we measured cAMP and cGMP (RIA); in hVSMC incubated with insulin and ionomycin we measured NO, evaluated as l-(3H)-citrulline production from l-(3H)-arginine; by northern blot hybridization, we measured the expression of cNOS mRNA. Results. i) By incubating hVSMC with 2 nmol/l insulin for 0–240 min, we observed an increase of both cGMP and cAMP (ANOVA: p = 0.0001). Cyclic GMP rose from 0.74 ± 0.01 to 2.62 ± 0.10 pmol/106 cells at 30 min (p = 0.0001); cAMP rose from 0.9 ± 0.09 to 11.65 ± 0.74 pmol/106 cells at 15 min (p = 0.0001). ii) Sodium nitroprusside (100 μmol/l) and glyceryltrinitrate (100 μmol/l) increased both cGMP and cAMP (p = 0.0001). iii) The effects of insulin on cyclic nucleotides were blocked by NOS inhibition. iv) An increase of NO was observed by incubating hVSMC for 5 min with 2 nmol/l insulin (p = 0.0001). v) Ionomycin (1 μmol/l) enhanced NO production (p = 0.0001) and increased both cyclic nucleotides (p = 0.0001). vi) hVSMC expressed mRNA of cNOS. Conclusion/interpretation. Human VSMC express cNOS, which is rapidly activated by insulin with a consequent increase of both cGMP and cAMP, suggesting that insulin-induced vasodilation in vivo is not entirely endothelium-mediated. [Diabetologia (1999) 42: 831–839]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051234
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  • 6
    Electronic Resource
    Electronic Resource
    Metformin reduces insulin requirement in Type 1 (insulin-dependent) diabetes (1983)
    Springer
    Diabetologia 24 (1983), S. 351-354 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 diabetes ; biguanides ; metformin ; insulin receptors ; insulin therapy ; artificial pancreas ; Biostator
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of metformin on Type 1 (insulin-dependent) diabetes has been assessed with the artificial pancreas. Fourteen Type 1 diabetic patients of normal body weight received in addition to their usual insulin therapy 850 mg metformin or placebo three times a day for 4–6 weeks. The sequence was placebo-metformin in eight patients and metformin-placebo in the other six. On the last day of metformin or placebo treatment, an artificial pancreas was used for about 36 h to assess insulin requirement. There was a 25.8% reduction in insulin requirement during metformin management despite slightly lower blood glucose levels (5.25±0.20 versus 5.98±0.18 mmol/l, P〈0.01). Maximum reduction (about 50%) occurred 2 h after both lunch and dinner. There was no nocturnal effect. A marked decrease in specific insulin binding before metformin was found (0.56 + 0.27% to 107 monocytes versus 2.82±0.75 of control subjects) and significant increase after metformin (1.36±0.36%, p〈0.05). There were no significant changes in blood lactate, total and HDL-cholesterol, triglycerides and C-peptide levels. These results show that insulin receptor binding is diminished in Type 1 diabetes, perhaps as a consequence of higher peripheral blood insulin levels and that metformin can improve binding, and so reduce the amount of insulin needed to reach euglycaemia. The insulin sparing effect is greatest after meals, and interference with intestinal absorption of sugars may also be important. It follows that metformin could be usefully administered to Type 1 diabetic patients with unimpaired liver and renal function to reduce their insulin requirement.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00251823
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  • 7
    Electronic Resource
    Electronic Resource
    Occurrence of low blood glucose concentrations during the afternoon in Type 2 (non-insulin-dependent) diabetic patients on oral hypoglycaemic agents: importance of blood glucose monitoring (1991)
    Springer
    Diabetologia 34 (1991), S. 662-667 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; hypoglycaemia ; oral hypoglycaemic agents ; blood glucose profiles ; monitoring protocols
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The European NIDDM Policy Group states that the lowest target for good control of Type 2 (non-insulin-dependent) diabetic patients is a blood glucose level 4.4 mmol/l, both fasting and postprandially. The aim of this study is to evaluate the occurrence and temporal distribution of values under this target in the clinical records of 463 Type 2 diabetic patients, treated by diet or diet and oral hypoglycaemic agents, monitored for at least 2 years. The protocol includes blood glucose measurements after overnight fasting (08.00 hours), 120–150 min after breakfast (11.00 hours) and 120 and 240 min after lunch (14.00 and 16.00 hours). At least one blood glucose concentration of less than 4.4 mmol/l was presented by 42% of the patients. The only difference between patients showing and not showing glycaemic levels under this target was the higher percentage on oral hypoglycaemic agents in the first group (68.4% vs 56.9%, p=0.016). We considered 299 blood glucose profiles containing at least one value of less than 4.4 mmol/l, observing that a) 46.9% of profiles from patients treated by diet alone and 68.7% of profiles from patients treated both by diet and oral hypoglycaemic agents presented the lowest blood glucose concentration at 16.00 hours (p=0.002). b) No correlation existed between fasting blood glucose and values at 16.00 hours in profiles from diet-treated patients, whereas a negative correlation was present in patients on diet and oral hypoglycaemic agents, indicating that an excess of oral agents, administered to correct fasting hyperglycaemia. was the cause of the low glycaemic values in the afternoon. c) 37.9% of profiles on a diet and 83.3% of profiles on diet and oral agents showed fasting glucose concentrations 〉6.7 mmol/l, the upper limit of good control according to the European NIDDM Policy Group. This indicates that fasting hyperglycaemia does not exclude the occurrence of low glucose values throughout the day and that it is necessary to monitor blood glucose profiles.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400996
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  • 8
    Electronic Resource
    Electronic Resource
    Insulin increases cyclic nucleotide content in human vascular smooth muscle cells: a mechanism potentially involved in insulin-induced modulation of vascular tone (1995)
    Springer
    Diabetologia 38 (1995), S. 936-941 
    Details
    ISSN: 1432-0428
    Keywords: Insulin ; arterial hypertension ; vasodilation ; vascular smooth muscle cells ; cyclic adenosine monophosphate ; cyclic guanosine monophosphate ; nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been suggested that insulin exerts a vasodilating effect, but the mechanisms involved are not completely understood. Since cyclic nucleotides mediate the vasodilation induced by endogenous substances, such as prostacyclin and nitric oxide, we aimed to investigate the influence of insulin (concentration range 240–960 pmol/l) on both cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) content in human vascular smooth muscle cells. Insulin dose-dependently increased both nucleotides (cAMP: from 0.7±0.1 to 2.6±0.4 pmol/106 cells, p=0.0001; cGMP: from 1.3±0.2 to 3.4±0.7 pmol/106 cells, p=0.033). This increase is receptor-mediated, since it was blunted when cells were preincubated with the tyrosine kinase inhibitor genistein. The effect of insulin remained significant (p=0.0001) when preincubation with the phosphodiesterase inhibitor theophylline prevented cyclic nucleotide catabolism. The increase of cGMP was blunted when the cells were preincubated with the guanylate cyclase inhibitor methylene blue, and with the nitric oxide-synthase inhibitor NG-monomethyl-l-arginine. At all the concentrations tested, insulin potentiated the increase of cAMP induced by the stable prostacyclin analogue Iloprost (p=0.0001), whereas only at 1920 pmol/l did it potentiate the cGMP increase induced by glyceryltrinitrate (p=0.05). This study demonstrates that the vasodilating effects exerted by insulin may at least in part be attributable to an increase of both cGMP and cAMP via a receptor-mediated activation of adenylate and guanylate cyclases in human vascular smooth muscle cells and that the insulin effect on cGMP is mediated by nitric oxide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400582
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  • 9
    Electronic Resource
    Electronic Resource
    Influence of protamine on adhesion, chemotaxis and proliferation of human vascular smooth muscle cells (1997)
    Springer
    Diabetologia 40 (1997), S. 67-75 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Protamine ; insulin ; heparin ; vascular smooth muscle cells ; diabetic angiopathy ; atherosclerosis.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been shown that, in streptozotocin diabetic rats, protamine-retarded insulin administered in vivo stimulates intimal hyperplasia in balloon-injured carotid artery. The aim of this study was to evaluate the influence of protamine on cultured human vascular smooth muscle cells (hVSMC), by observing its effects on adhesion, chemotaxis and proliferation. hVSMC were isolated during abdominal surgery, cultured and utilized at passages 6–10. We observed that protamine stimulates: 1) cell adhesion in the concentration range 0.04–20 μg/ml (analysis of variance, ANOVA, p 〈 0.0001); 2) cell chemotaxis in the absence of fetal calf serum (FCS) in the concentration range 1–200 μg/ml (ANOVA, p 〈 0.0001) and in the presence of 1 % FCS in the concentration range 5–200 μg/ml (ANOVA, p 〈 0.0001), further enhancing the chemotaxis induced by 10 % FCS in the concentration range 20–200 μg/ml (ANOVA, p 〈 0.0001); 3) cell proliferation and 3H-thymidine incorporation from 1 to 5 μg/ml (ANOVA, p 〈 0.0001); 4) cell c-fos oncoprotein nuclear expression. We also observed that protamine effects on chemotaxis, proliferation and c-fos expression are inhibited by heparin that human insulin stimulates cell proliferation and 3H-thymidine incorporation (ANOVA, p 〈 0.0001) at concentrations equal to or greater than 480 pmol/l and that these effects of insulin persist in the presence of protamine. In conclusion, protamine influences hVSMC behaviour by interfering with biological functions involved in atherogenesis. The concentrations used in this short-term in vitro study were higher than those probably occurring in vivo in patients chronically treated by protamine-retarded insulin preparations: further studies, therefore, are needed to evaluate the safety of protamine as a retardant of insulin action in vivo. [Diabetologia (1997) 40: 67–75]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050644
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