Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A comparative cross-over trial of mefruside and cyclopenthiazide, each drug being given for 6 weeks, was conducted on thirty hypertensive patients with diabetes mellitus or impaired glucose tolerance. Other antihypertensive therapy, any antidiabetic therapy and potassium supplementation were kept constant throughout the trial. Dosages of mefruside and cyclopenthiazide were adjusted to give approximately equal blood pressure levels in the two drug periods. 2. There was no significant difference in the following parameters studied during the sixth week of each of the two periods of drug therapy: serum electrolytes, total CO2, chloride, urea, amylase, haemoglobin, erythrocyte sedimentation rate, platelet and white blood cell counts, lying and standing blood pressure and pulse rate, weight, fasting and 2-h glucose and insulin levels and five-value glucose and insulin curve areas, fasting calcium and phosphate. 3. Serum creatinine and uric acid showed a small but significant fall during mefruside therapy.
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PMID:Effect of equivalent antihypertensive doses of mefruside and cyclopenthiazide on serum electrolytes, uric acid and glucose tolerance in hypertensive patients. 109 62

A 15-month-old girl was successfully treated for substantial hyperosmolarity in the absence of ketosis at the onset of permanent insulin-requiring diabetes mellitus. Hypotonic solutions containing small amounts of glucose and subcutaneous administration of low doses of insulin were empolyed. Potassium was added to the hydrating solutions during the second hour of treatment. In the next three months, two recurrences of this syndrome were verified and successfully treated in a similar manner.
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PMID:Recurrent hyperosmolar nonketotic episodes in a young diabetic. 111 59

The effects of low-mineral content water (Adelholzener Primus-Quelle) in 62 patients were studied of which 14 were hypertonic. Changes of blood sodium, potassium, chloride and bicarbonate were not observed in either group. In the hypertonic patients, blood pressure decreased from a mean systolic value of 168 to 140 mmHg and mean distolic pressure from 105 to 88 mmHg. Observations to date suggest the following indications for a low-mineral content water diet: 1. hypertension, 2. renal insufficiency in stages of compensated and decompensated retention, especially in cases with high serum potassium levels, 3. in the initial therapy of diabetes, gout and obesity; patients with a high water demand should be treated with low-mineral content water until the optimal intake of electrolytes is established.
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PMID:[Effects of water with a low mineral content on serum electrolytes and blood pressure]. 122 36

A method of radiometry of the whole body in the low-background chamber was applied to the study of the content of total potassium (by K40) in the organism of 67 patients suffering from diabetes mellitus of various severity and in 76 healthy individuals. there was revealed a marked reduction of the total potassium level in diabetics. The more severe the diabetes--the greater the potassium deficiency. Total potassium level had a tendency to normalization after treatment with insulin, potassium salts and vitamins.
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PMID:[Potassium metabolism in diabetes mellitus]. 122 45

The problem of the association between adult diabetes, obesity and manic-depressive psychosis is examined in the light of new endocrinological and psychopharmacological findings. After a critical review of the vast old and recent literature on the matter, a physiopathological interpretation of the clinical association is put forward on the basis of mental, nervous and endocrine correlations in carbohydrate metabolism, with special reference to manic-depressive psychosis. The insulin-like effect of lithium on carbohydrate metabolism and correlated ions (phosphates, calcium, magnesium, potassium) at cell membrane level is then discussed. Theoretical and practical conclusions are drawn on the basis of these data. The former propose an essentially "structural" or "intersection" hypothesis of the association and suggest depth study of the insulin function especially in the "normal" phase of manic-depressive psychosis. The latter show the possibility of a clinical trial with lithium and other anti-depressant drugs in obese diabetics, with a close cooperation between psychiatrist and diabetologist.
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PMID:[Introduction to new research on correlations between manic-depressive psychosis and adult obesity-linked diabetes]. 123 Jan 36

Insulin secretion by the pancreatic Beta cell is dependent upon transmembrane ion fluxes gated by the ATP-regulated potassium channel and the voltage regulated, L-type calcium channel. This work group examined major recent advances in the structure and modulation of ion channels and how those advances may pertain to the physiology of insulin secretion and the pharmacological treatment of Type 2 (non-insulin-dependent) diabetes mellitus. Structural studies have revealed that voltage gated ion channels are related, complex, and comprised of multiple components: sodium channels consist of three distinct subunits. L-type calcium channels, crucial to the insulin secretory response are structurally related to the sodium channel but contain additional subunits. Potassium channels are less closely related and appear to function as homotetramers. Modulation of ion channel activity is similarly complex: site specific phosphorylation by multiple protein kinases under the control of several intracellular second messenger systems may increase or decrease conductance. Subunit composition and relatively stable changes in the modal state of ion channels also appear to be critical to ion channel gating properties. Functional studies of the Beta-cell ATP-regulated potassium channel suggest two distinct nucleotide binding sites which link this channel to the metabolic state of the Beta cell. The multiple paths of ion channel modulation provide multiple targets for therapeutic intervention. Where detailed characterisation of ion channel structure has been achieved, those targets are being used for specific drug design. Such complete characterisation has not yet been achieved for Beta-cell ion channels and this presents a major goal for diabetes research.
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PMID:Ion channels. 128 78

The purpose of the present study was to assess the efficacy and tolerability of diuretic-free antihypertensive therapy with a calcium antagonist and/or an angiotensin converting enzyme (ACE) inhibitor in patients with diabetes mellitus. 54 hypertensive [blood pressure (BP) above 140/90mm Hg] patients with diabetes mellitus type 1 (n = 7) or 2 (n = 47) and normal serum creatinine levels (mean 82 +/- 6 mumol/L) received either verapamil or enalapril after a 2-week washout and a 4-week placebo phase. If BP remained elevated, both agents were combined. Verapamil or enalapril alone normalised diastolic BP (to less than 90mm Hg) in 36 patients; verapamil decreased BP from 159/98 to 147/87mm Hg (n = 19, p < 0.001) and enalapril decreased BP from 166/99 to 146/88mm Hg (n = 17, p < 0.001). In 18 patients who remained hypertensive after 10 weeks of monotherapy, a combination of both drugs decreased BP from 169/104 to 151/90mm Hg (p < 0.001). Overall, 87% of patients achieved a target BP response at 30 weeks. Urinary albumin as related to creatinine excretion (UAE; micrograms albumin:mg creatinine) was on average not significantly changed after verapamil or enalapril treatment, alone or combined. Nevertheless, in patients with initial microalbuminuria, UAE decreased (p < 0.05) during enalapril treatment. Serum potassium, total lipids, high density lipoprotein cholesterol, low density lipoprotein cholesterol, glycosylated haemoglobin, serum C peptide and fructosamine levels were not significantly modified by treatment. Subjective tolerability of the drugs was also generally good. Thus, in hypertensive patients with diabetes, a diuretic-free therapy based on the calcium antagonist verapamil or the ACE inhibitor enalapril, alone or combined, can effectively decrease BP without adversely affecting carbohydrate and lipid metabolism.
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PMID:Swiss hypertension treatment programme with verapamil and/or enalapril in diabetic patients. 128 88

During the past decade, it became obvious that in contrast to defective insulin secretion in type I diabetes, defective insulin action (insulin resistance) is the most pertinent feature of type II diabetes. In addition, it has been known for a long time that obesity and insulin resistance are closely linked. Recently, hypertension also has been shown to often coincide with insulin resistance, although any causal relationships are still hypothetical. Last, several widely used pharmacological drugs such as diuretics, adrenergic blockers, and angiotensin-converting enzyme inhibitors may influence insulin sensitivity. Therefore, growing interest has emerged to most accurately measure insulin sensitivity. Although considerable knowledge has accumulated as to the actual mechanisms of insulin-dependent glucose transport, the signal transduction pathway of insulin remains poorly understood. When insulin sensitivity is measured, it is the overall glucose uptake that is quantified under controlled conditions. Other actions of insulin, such as the transport of ions, (e.g., sodium and potassium), synthesis of insulin-like growth factor-binding proteins, translocation of transporter proteins, and regulation of enzyme activities, are much more difficult to quantify. Of the many approaches used to quantify insulin action, the euglycemic hyperinsulinemic clamp technique has emerged as the most reliable tool, fulfilling clinical and scientific demands equally. In combination with tracer methodology and calorimetry, a detailed view into the quantitative aspects of insulin action at different target cells is possible. Whether insulin resistance extends to other known actions of insulin in addition to those on glucose metabolism remains open to debate.
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PMID:Determination of insulin sensitivity: methodological considerations. 128 39

Treatment with thiazide diuretics causes impaired glucose tolerance, biochemical diabetes, and insulin resistance. The effect of diuretics on glucose tolerance is clearly dose-related. Spironolactone does not impair glucose tolerance, even at high dosage, but differences among other diuretics could be due to comparisons at doses that are not equal. Diuretic-induced changes in glucose metabolism are not conclusively related to altered potassium homeostasis, and impaired glucose tolerance occurs even when relatively low doses of thiazide are combined with potassium-sparing agents. The effects of diuretics on glucose homeostasis are in large part and probably entirely reversible. These disturbances of glucose metabolism have been detected only by detailed biochemical testing, and their clinical relevance is uncertain. In established diabetes, diuretics have a rapid and substantial adverse effect on metabolic control. In nondiabetic subjects, diuretics rarely cause or trigger a serious hyperosmolar nonketotic diabetic syndrome. Otherwise, it is not known whether the metabolic changes cause clinical diabetes or lead to microvascular complications in the long term. Evidence from large outcome trials suggests that biochemical diabetes, glucose intolerance, and insulin resistance do not increase the risk of coronary heart disease in treated hypertensive patients. Diuretics should be avoided in patients with diabetes unless their use is essential. Otherwise, a low dose of thiazide remains as excellent choice for first-line antihypertensive therapy. Dihydropyridine calcium antagonists, diltiazem, and verapamil appear to have no important effects on glucose homeostasis. There is very limited evidence that selective alpha-antagonists increase insulin sensitivity. The importance of metabolic differences between drug classes will be established only by comparative outcome trials with coronary events as the end point.
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PMID:Influence of diuretics, calcium antagonists, and alpha-blockers on insulin sensitivity and glucose tolerance in hypertensive patients. 128 44

Fasting plasma glucose levels, serum osmolality and serum concentrations of sodium and potassium were determined in 73 Libyan diabetic patients attending the outpatient clinic of the Diabetes Hospital, Tripoli, Libya. The respective mean values were 234.8 +/- 9.7 mg.dl-1, 288.5 +/- 2 m0sm.L-1, 134.7 +/- 0.8 mEq.L-1 and 4.2 +/- 0.07 mEq.L-1. Statistically significant correlations were present between fasting plasma glucose and serum osmolality as well as the concentrations of serum sodium and potassium. There is is an increase in osmolality and levels of sodium and potassium concentration with an increase in plasma glucose concentration.
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PMID:Serum electrolytes and osmolality in diabetes mellitus. 129 47


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