{"title":"The insulin-antagonistic effect of the counterregulatory hormones.","authors":"I Lager","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The counterregulatory hormones glucagon, adrenaline, cortisol and growth hormone are released during hypoglycaemia, and under other stress conditions. These hormones have insulin-antagonistic effects both in the liver and in the peripheral tissues. The insulin-antagonistic effects of glucagon and adrenaline are of rapid onset, whereas those of cortisol and growth hormone are only observed after a lag period of several hours. Glucagon is the most important hormone for acute glucose counterregulation. When the release of this hormone is deficient, as in patients with insulin-dependent diabetes, adrenaline becomes the most important hormone for glucose recovery during hypoglycaemia. Cortisol and growth hormone contribute to counterregulation during prolonged hypoglycaemia, but adrenaline is also of utmost importance in this condition. Adrenaline induces the early posthypoglycaemic insulin resistance, whereas cortisol and growth hormone are important for the insulin resistance that is observed later following hypoglycaemia. However, the importance of posthypoglycaemic insulin resistance for induction of posthypoglycaemic hyperglycaemia in clinical situations is limited. The pronounced insulin-antagonistic effect of growth hormone indicates that this hormone, in addition to its effect on the dawn phenomenon, could also play a key role in the regulation of other diurnal rhythms of glucose metabolism.</p>","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"735 ","pages":"41-7"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13199290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hypertension and glucose tolerance--effects of antihypertensive therapy.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"735 ","pages":"1-128"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13199285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hypertension as a metabolic disorder--an overview.","authors":"U Smith, S Gudbjörnsdottir, K Landin","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hypertension is related to several conditions with abnormalities in carbohydrate and lipid metabolism, such as obesity and impaired glucose tolerance. However, perturbed metabolism is also seen in non-obese hypertensive individuals. In addition, hypertension is linked to impaired fibrinolysis and elevated levels of the plasminogen activator inhibitor of endothelial type (PAI-1). Insulin resistance and hyperinsulinaemia in essential hypertension may be an important cause of these metabolic and fibrinolytic abnormalities. Whether hyperinsulinaemia is the cause of hypertension is currently unknown. However, it is clear that the relationship between hypertension and insulin is complex, and further studies are required to clarify this association. Based on the evidence states, it is suggested that insulin resistance and hyperinsulinaemia play a role in hypertension. However, it is also clear that hyperinsulinaemia occurs in the absence of hypertension, which suggests that other factors, such as genetic susceptibility, may be important.</p>","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"735 ","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13199286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolic effects of ACE inhibitors.","authors":"C Berne","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>More than 10 years of clinical experience using angiotensin-converting-enzyme (ACE) inhibitors have shown that this class of drug does not have any adverse metabolic effects on carbohydrate and lipid metabolism. Rather, a number of studies on patients with essential hypertension or non-insulin-dependent diabetes mellitus have indicated minor improvements in glucose homeostasis and correction of dyslipidaemia. Some recent studies using the euglycaemic insulin clamp technique have indicated that the beneficial effect of captopril, the most extensively studied drug, is exerted on insulin sensitivity, a site with the potential to influence glucose and lipid metabolism. There is no uniform explanation for this action of captopril, but increased blood flow in skeletal muscle, accumulation of bradykinin or more efficient insulin release may be suggested as potential modes of action. It remains to be established whether this effect of captopril can be extrapolated to other ACE inhibitors, and the extent to which effects on insulin sensitivity will influence the long-term consequences for future risk of diabetes mellitus and coronary heart disease in patients with essential hypertension.</p>","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"735 ","pages":"119-25"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13199288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolic effects of antihypertensive treatment with beta-blockers.","authors":"P T Sawicki, M Berger","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The beneficial effects of beta-blockers on morbidity and mortality have been demonstrated in several prospective long-term trials. The suspected negative metabolic effects of low-dose beta 1-selective-blockers do not appear to be relevant to daily clinical practice, and do not restrict the use of these agents as first choice antihypertensive drugs in diabetic or non-diabetic patients.</p>","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"735 ","pages":"97-9"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12839665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mechanisms involved in the regulation of the insulin secretory process.","authors":"S Efendic, H Kindmark, P O Berggren","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"735 ","pages":"9-22"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12811433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Insulin resistance in hypertension--a relationship with consequences?","authors":"C Berne","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Resistance to the action of insulin on glucose metabolism, with the ensuing compensatory hyperinsulinaemia, is closely linked to essential hypertension. The decreased insulin sensitivity observed in hypertensive patients is independent of obesity. Hyperinsulinaemia is likely to promote the dyslipidaemia that frequently accompanies the hypertensive state, and often presents as increased total and very low density lipoprotein (VLDL)-triglycerides, low high density lipoprotein (HDL)-cholesterol and, in some studies, elevated levels of low density lipoprotein (LDL)-cholesterol. Lipid abnormalities, hypertension and possibly hyperinsulinaemia act together to increase the risk of atherosclerotic disease manifestations in hypertensive patients. Acutely, insulin has been shown to stimulate sympathetic nervous system activity and transmembrane electrolyte transport, to promote sodium retention and to cause vascular wall changes, including increased cholesterol biosynthesis and smooth muscle proliferation. If these mechanisms operate on a chronic basis, the continuous exposure to elevated plasma insulin levels may play a pathogenetic role in the development of high blood pressure, and also of a predisposition toward atherosclerosis in patients with hypertension. Further studies are necessary to establish these hypothetical cause-effect relationship which, if shown to be true, will contribute to a more wide-ranging view of essential hypertension and the optimum strategy for antihypertensive treatment.</p>","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"735 ","pages":"65-73"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13199157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Contribution of estimated insulin resistance and glucose intolerance to essential hypertension.","authors":"K F Eriksson, F Lindgärde","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In a population study of 6956 middle-aged men, 5% received drug treatment for hypertension, another 25% had a blood pressure of greater than 160.90 mmHg, and 3.2% were diabetic. Prevalence of impaired glucose tolerance and diabetes was two- to threefold in hypertensive subjects, and 50% of the glucose intolerant or diabetic cases had hypertension. In 4677 unselected subjects without clinical coronary heart disease or previous diabetes, estimated insulin resistance (i.e. the 2-h insulin-to-glucose ratio during an oral glucose tolerance test, controlled for body mass index) correlated with both systolic and diastolic blood pressure. In untreated subjects, a diastolic blood pressure of greater than 90 mmHg was found in conjunction with a higher insulin resistance value than predicted, whereafter blood pressure progressively increased. The contribution of drug treatment to insulin resistance was significant, but less than 1% in the whole material and about 2.5% in cases with impaired glucose tolerance.</p>","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"735 ","pages":"75-83"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13199158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M Risenfors, M Hartford, M Dellborg, R Luepker, A Hjalmarsson, K Swedberg, S Holmberg, J Herlitz
{"title":"Effect of early intravenous rt-PA on infarct size estimated from serum enzyme activity: results from the TEAHAT Study.","authors":"M Risenfors, M Hartford, M Dellborg, R Luepker, A Hjalmarsson, K Swedberg, S Holmberg, J Herlitz","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In 319 patients who participated in a double-blind trial to evaluate the effect of early rt-PA administration compared to placebo in suspected acute myocardial infarction, infarct size was assessed from analyses of serum activity of lactate dehydrogenase isoenzyme 1 (LD 1). Treatment was always started less than 3 h after the onset of symptoms, with one-third of the patients' treatment being initiated outside the hospital. The maximum activity of LD 1 was reduced by 32%, from 13.3 mu kat l-1 in placebo to 9.0 mu kat l-1 in rt-PA treated patients (P = 0.001). A reduction in LD-1 activity after rt-PA treatment was restricted to patients with ST-elevation in the initial electrocardiogram, and was more pronounced in patients with previous ischaemic heart disease, above median age, and in those with a shorter delay in initiation of treatment. We conclude that very early intravenous treatment with rt-PA limits indirect signs of infarct size. The effect appears to be restricted to patients with ST-segment elevation in their initial electrocardiogram.</p>","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"734 ","pages":"11-8"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13059752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M Risenfors, I Zukauskiene, P Albertsson, M Hartford, M Lomsky, J Herlitz
{"title":"Early thrombolytic therapy in suspected acute myocardial infarction--role of the electrocardiogram: results from the TEAHAT Study.","authors":"M Risenfors, I Zukauskiene, P Albertsson, M Hartford, M Lomsky, J Herlitz","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In a placebo-controlled trial in which rt-PA was administered to patients within 2 h and 45 min after the onset of symptoms indicative of acute myocardial infarction (AMI), 352 patients were randomized. Standard 12-lead electrocardiograms (ECGs) were recorded at inclusion and repeatedly during admission and at follow-up after 1 month and 1 year. In patients who presented with ST-segment elevation, the infarction rate was high (88%), whereas in patients without ST-elevation the infarction rate was low (21%), and infarct size, as assessed by serum enzyme activities, was small in this group. There were only minor differences between rt-PA- and placebo-treated patients with regard to ST-segment changes and Q-wave development, whereas the R-wave amplitude was higher after 1 month in patients who were given rt-PA. The infarction rate was not altered by rt-PA, but there was a shift towards a reduction in Q-wave infarction in patients who were treated with rt-PA. When a score system, as suggested by Palmeri et al., intended to reflect the ultimate infarct size, was applied, a significantly lower score was found in infarction patients who were treated with rt-PA as compared to placebo (3.95 +/- 0.35 vs. 2.95 +/- 0.29, P = 0.03), indicating limitation of infarct size. In summary, early treatment with rt-PA resulted in less frequent Q-wave infarction and a reduction in the electrocardiographically estimated infarct size.</p>","PeriodicalId":77556,"journal":{"name":"Journal of internal medicine. Supplement","volume":"734 ","pages":"19-25"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13059753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}