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The proposition that lifestyle is a major determinant of community health is explored by contrasting the features of a rural subsistence community in the highlands of Papua New Guinea and the features of the community in urbanized, industrialized Australia. Reference is made to differences in physical environment, housing, work, social situation, human relationships, patterns of disease, population statistics, diet, growth, obesity, physical fitness, blood lipid concentrations, blood pressure, salt intake and the occurrence of hypertension, diabetes, cardiovascular disease and signs of degenerative changes in various tissues. The Papua New Guinea community is seen as a self-reliant, self-contained, socially cohesive subsistence society whose members are well adapted to their physical and social environment, free from major degenerative cardiovascular diseases, with little overt psychiatric illness, but with a heavy burden of infectious disease, with marginal nutritional levels of degenerative disease and disease from psychological stress. It is clear that health, in its fullest sense, is not the prerogative of any one type of society.
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PMID:Lifestyle, health and disease: a comparison between Papua New Guinea and Australia. 73 10

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
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PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48

The renin-angiotensin-aldosterone system was evaluated in two types of uncontrolled diabetes: a) diabetic ketoacidosis, and b) nonketotic hyperglycemia. In thirteen patients with ketoacidosis, mean plasma renin activity (PRA) was 58 plus or minus 12 (S.E.M.) ng. per milliliter per hour and in four patients, plasma aldosterone was 82 plus or minus 17 ng. per 100 ml. Corresponding values for upright salt-depleted subjects were 13 plus or minus 2 and 62 plus or minus 8. In eleven diabetics with nonketotic hyperglycemia (mean glucose 318 plus or minus 19 mg. per cent), mean blood volume was 4,660 ml. and PRA 2.1 plus or minus .7. After control of the diabetes (mean glucose 129 plus or minus 13) blood volume was 4,553 ml. and PRA 3.3 plus or minus 1 (NS). The results suggest that: 1) diabetic ketoacidosis is a state of severe secondary aldosteronism, 2) no significant change in blood volume or PRA occurs during short periods of hyperglycemia, and 3) insulin is not necessary for renin release.
Diabetes 1975 Feb
PMID:Plasma renin activity and blood volume in uncontrolled diabetes. Ketoacidosis, a state of secondary aldosteronism. 80 22

A new automated potentiometric method for the determination of colipase was developed, taking advantage of the reactivation of purified lipase, in the presence of bile salt and at pH 6.5. High-fat and high-starch diets induced an opposite regulation of lipase and amylase in the rat pancreas. At the same time, the level of colipase was not influenced by nutrition. During fasting and in alloxan diabetes, the specific activity of lipase almost doubled, that of amylase decreased sharply, and colipase was not affected in the rat pancreas. In obese-hyperglycemic mice, suffering from obesity, hyperinsulinism, and moderate diabetes, there was also no regulation of pancreatic colipase. Thus, at variance with a number of hydrolases, there was no dietary or hormonal adaptation of colipase. However, this was probably without any bearing on intraluminal lipolysis. Indeed, comparison of lipase and colipase activities in pancreas and in small intestine suggests that colipase concentration is not a limiting factor of intraluminal lipolysis. The molecular mechanism of this assumption is discussed on the basis of in vitro studies.
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PMID:Lack of adaptation of pancreatic colipase in rats and mice. 84 20

Statistics from various studies are compiled to present an overview of the somatic complications of induced abortions. These complications are divided into 2 groups, the 1st consisting of ''early'' complications that arise during the abortion or for 30 days afterwards. From 1970 to 1974, 1-9 deaths/100,000 induced abortions are registered in studies from various countries. A study from England and Wales shows that patient deaths after abdominal uterotomy are 3-9 times more numerous than vacuum and instrumental evacuation of the uterus and that abortions performed after the 12th week are 1.25-4.0 times more prevalent than during the first 12 weeks. ''Early'' complications are then divided into 2 categories, ''serious complication,'' e.g., uterine perforation, loss of blood requiring a transfusion, and ''complication'' exemplified by pyrexia. In various studies from throughout the world, ''complications'' arose in 4-25.6% of the cases and ''serious complications'' in 1.1-7.6%. In women with a somatic illness (e.g., diabetes) during an abortion, a greater percentage have complications. Patients having extirpation of the uterus, uterotomy, and sterilization, or salt water instillation had at least 3 times as many complications as those having vacuum aspiration or dilatation and curettage. The 2nd type of complication, the ''late'' complications, are permanent (e.g., sterility), or occur 30 days after the abortion (e.g., endometriosis). These complications are generally poorly documented and researched. The frequency of sterility as a ''late'' complication ranges from 1-6% in 1 study to 53% in another. There are indications that previous induced abortion can cause premature birth or spontaneous abortion, although there is contradicting evidence. These ''late'' complications are caused by cervical insufficiency caused by the induced abortion. More documentation is needed to make statements about the ''late'' complications.
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PMID:[Somatic complications following induced abortions]. 125 10

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
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PMID:Hypertension and insulin resistance. 128 47

Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antihypertensive therapy in diabetic patients. 128 10

Fusidic acid and its sodium salt (fusidin) are anti-staphylococcal drugs. In vitro studies have shown that they prevent the lymphocyte co-stimulatory activities of the cytokines IL-1 and IL-6 in a manner similar to that of cyclosporin A, and prevent the inhibitory effect of IL-1 on glucose-induced insulin production. As IL-1 and IL-6 are thought to play a role in the pathogenesis of Type 1 diabetes, the aim of this study was to investigate whether fusidin could influence the disease incidence of the spontaneously diabetic BB rat model. Accordingly, a group of 50 BB rats receiving fusidin dissolved in their drinking water were compared to a control group of 55 rats over a period of 200 days. The incidence of diabetes was found to be 52% in the experimental group and 71% in the control group (P < 0.05). The degree of insulitis and the number of islets at histological examination were similar among the non-diabetic animals whereas the diabetic fusidin-treated animals showed a higher degree of islet preservation than the diabetic control rats. The results are highly indicative of an anti-diabetogenic effect of fusidin.
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PMID:Anti-diabetogenic effect of fusidic acid in diabetes prone BB rats. 130 76

During a 4-year period, acute renal failure was observed in 27 patients (mean age 65 years) treated by various angiotensin-converting-enzyme (ACE) inhibitors for hypertension, heart failure, or a combination of both. None had significant renal artery stenosis on angiography. Overt volume depletion was present in 21 and hypotension in 12 cases. All patients received diuretic therapy and/or a low-salt diet. Other facilitating factors included cardiac failure, pre-existing chronic renal insufficiency, combined therapy with non-steroidal anti-inflammatory drugs, and diabetes mellitus. Twenty-two patients had two or more of these factors at presentation. A renal biopsy performed in 10 cases showed severe arteriosclerosis of small renal arteries in eight and acute tubular necrosis in five instances. Therapy comprised volume expansion, and withdrawal of diuretics and, except in two patients, of ACE inhibitors. Twenty-one patients recovered normal renal function, two died, and permanent renal damage remained in four. These results suggest that sodium depletion has a critical role in inducing acute renal failure, whose outcome is not always benign. A combination of diuretics and ACE inhibitors should be prescribed with caution, especially in older patients with small as well as with large renal vessel disease.
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PMID:Acute renal failure after the use of angiotensin-converting-enzyme inhibitors in patients without renal artery stenosis. 131 66

High blood pressure of unknown etiology has been related to many pathogenetic factors, mainly dietary salt intake, mental stress, alcohol consumption, sedentary living and aging. Hypertension is more common in condition such as obesity and diabetes mellitus. Sustained elevation of arterial pressure is mediated by vasoconstriction in response to catecholamine release and activation of the renin-angiotensin-aldosterone system. In obese and diabetic subjects, insulin resistance and hyperinsulinemia have been found to be related to development of hypertension. The hypertension phenotype may correspond to many different genotypes codifying various alterations of hormone and receptor function, as well as inherited diseases linked to hypertension. An outstanding epidemiologic example of how hypertension may appear in a community is found in Easter Island. Hypertension among native adults increased from 3 to 30% in a 10 year period, in relation to influx of tourism and changes in salt intake and diet.
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PMID:[Etiopathogenic factors of arterial hypertension]. 134


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