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)

We used the fluorescent dye 2',7'-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF) to examine intracellular pH (pHi) regulation in single hepatocytes isolated from control rats and rats with either spontaneous or drug-induced diabetes mellitus (DM). In the absence of CO2-HCO3-, both control and DM cells recovered from cellular acid loads applied by the NH4+ prepulse technique. Because the pHi recovery was blocked by either Na+ withdrawal or ethylisopropylamiloride in both control and DM cells, it was presumably mediated by Na(+)-H+ exchange. In the control cells, the pHi threshold above which the rate of change of pHi (dpHi/dt) was zero was 7.06, and the slope of the dpHi/dt-pHi relationship was -0.030 s-1. In the DM cells, the pHi threshold was 7.22 and the slope was -0.017 s-1. Thus, at pHi values below approximately 6.9, the pHi recovery was slower in the DM cells. Inasmuch as we observed no difference in the cellular buffering power between control and DM cells, diabetes inhibits Na(+)-H+ exchange within this low pHi range. At pHi values above approximately 6.9, however, Na(+)-H+ exchange was apparently stimulated by diabetes. Thus diabetes induces two distinct alterations of Na(+)-H+ exchange, an alkaline shift in pHi threshold and decrease in slope. Treatment of diabetic rats with insulin for 48 h restored both Na(+)-H+ exchange parameters to normal. On the other hand, insulin added in vitro to DM cells for 2-5 h shifted the threshold toward the control value without affecting the slope, thus leading to a further inhibition of Na(+)-H+ exchange over the entire pHi range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of diabetes on Na(+)-H+ exchange by single isolated hepatocytes. 184 69

A 24-year-old newly diagnosed male patient with diabetes presented with diabetic ketoacidosis (DKA) (pH 7.16, HCO3 6.0) and extreme hypertriglyceridemia (239.35 mmol/L). The diagnosis of DKA was delayed because of the apparent depression of the true serum glucose (to 11 mmol/L). He was treated with intravenous (IV) insulin and rehydration, which normalized his pH, HCO3, and triglyceride levels. To the authors' knowledge, this is both the highest triglyceride level recorded and the first report of a high triglyceride level as the apparent cause of a factitiously low glucose level.
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PMID:Pseudonormoglycemia in diabetic ketoacidosis with elevated triglycerides. 189 2

A 59-year-old female patient was admitted because of muscle weakness in all four limbs for a period of 5 days. She had been found to have Graves' disease 4 years ago previous to this, and had received a subtotal thyroidectomy 1 year later. Hypothyroidism supervened and she had been receiving levothyroxine replacement in recent years. She also had non-insulin-dependent diabetes, which was controlled with diet only. During the 5 days prior to admission, she developed muscle weakness which finally worsened to complete paralysis of all four limbs. Physical examination showed tenderness and weakness of the extremity muscles. Abnormal laboratory data included serum K, 1.6 mEq/L; P, 1.2 mg/dl; uric acid, 1.6 mg/dl; fasting glucose, 267 mg/dl; T3, 36.65 ng/dl; T4, 4.0 micrograms/dl; TSH, 5.35 mu u/ml; free T4, 0.57 ng/dl; and metabolic acidosis with pH, 7.298; PCO2, 27.0 mmHg; and HCO3, 12.8 mEq/L. An EKG showed a prominent U wave, and urinalysis revealed renal glucosuria and massive aminoaciduria. An oral sodium bicarbonate loading test showed an increasing loss of bicarbonate through the urine, while the plasma bicarbonate level was elevated. Clinical manifestations improved after the administration of sodium bicarbonate, potassium chloride and neutral phosphate.
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PMID:Fanconi syndrome: report of a case. 198 86

We describe the clinical outcome of 13 patients with non-insulin-dependent diabetes mellitus (NIDDM), renal insufficiency, and proteinuria, treated for 12.2 +/- 12.9 months (mean +/- SD) with a low-protein, very-low-phosphorus diet (LPVLP) containing 30 g protein and 11.3 mmol (350 mg) phosphorus. After a control period of 18.2 +/- 20.4 months, LPVLP therapy was initiated and serum urea nitrogen, uric acid, and phosphate, as well as urinary excretion of protein, creatinine, urea nitrogen, uric acid, and phosphate, decreased significantly. There was no change in mean blood pressure, hemoglobin, blood pH, and HCO3-, as well as in serum creatinine, protein, albumin, calcium, magnesium, cholesterol, triglyceride, beta-lipoprotein, and high-density lipoprotein (HDL)-cholesterol. Nitrogen balances were measured over 5 weeks in nine patients. Nitrogen balance increased significantly from a negative balance of -0.795 +/- 1.367 g/d in the first week, to almost neutral in the fourth week, and later, was neutral or positive. Neither uremic symptoms nor signs of malnutrition appeared during the LPVLP period. These results suggest that negative nitrogen balance during the initial few weeks does not predict future nutritional status of patients with diabetic renal failure.
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PMID:Effect of low-protein, very-low-phosphorus diet on diabetic renal insufficiency with proteinuria. 206 52

This work describes a perfusion technique adapted to the isolated rabbit pancreas allowing investigation of both the endocrine and exocrine function. The pancreas-duodenum-stomach-spleen complex is removed and perfused with a modified Krebs Ringer Bicarbonate medium. The surgical steps leading to the removal of the complex are described. The endocrine response is studied by measuring insulin release when the pancreas is submitted to successive glucose stimulations and the exocrine function is evaluated by the alpha-chymotrypsin activity of the pancreatic juice harvested during the perfusion.
Diabetes Res 1990 Feb
PMID:An in vitro method for studying endocrine and exocrine secretion in the perfused isolated rabbit pancreas. 209 76

The clinical relevance of regular serum aluminium monitoring in dialysis patients was investigated in a multicentre study by 6-monthly determination of the serum aluminium during 4 consecutive years. In a group totalling 1193 patients, a striking decrease of mean serum aluminium was observed the last 2 years of the study. This phenomenon was accompanied by a substantial reduction of the prescribed dose of aluminium hydroxide (Al(OH)3) and its partial replacement by calcium carbonate (CaCO3) and/or magnesium hydroxide (Mg(OH)2). Under this policy serum phosphate control remained satisfactory. In all the centres, water treatment was found to be adequate, yielding dialysate aluminium around 2 micrograms/l. Dialysis patients with clinically overt liver disease showed a significantly greater median serum aluminium concentration than that observed in a control dialysis population. Compared to the latter group, the median serum aluminium concentration of dialysis patients with diabetes mellitus did not differ significantly. Results further indicated that patients with biopsy-proven osteomalacia presented a significantly greater median serum aluminium compared to that of patients without osteomalacia. We demonstrated that a serum aluminium of 60 micrograms/l provides a relatively sensitive (82%) and specific (86%) index for the detection of aluminium-related bone disease (ARBD). Provided the aluminium determinations are performed by a qualified laboratory, serum monitoring in dialysis patients (a) allows the safer use of aluminium-containing phosphate binders, and (b) is of value in the diagnosis of overload/toxicity.
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PMID:Value of serum aluminium monitoring in dialysis patients: a multicentre study. 131 84

We were checking the thermal waters of Varazdinske Toplice--sulfuric mineral calcium natrium hydrocarbonic sulfatic hyperthermic (t: 57.8 st. C, H2S: 8.1 mg/l, min: 955 mg/l mvol uk. 24.70 Ca: 50.12 mvol%, HCO3 54.12 mval%, SO4 26.18 mval%) on the sugar level in the patient's blood, suffering from Diabetes mellitus. We were following the state of 35 patients who were on the peroral therapy with the antidiabetics and ADA diet before coming in our hospital. We excluded the medication therapy at the beginning of the experiment. The patients were drinking 1200 ml of mineral water daily and spent 30 min bathing in the same water. The checking lasted 20 days in the average, and the level of GUK was measured every third day. The results are encouraging, further examinations are still lasting.
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PMID:[Use of the Varazdinske Toplice mineral water in the treatment of diabetes mellitus]. 213 62

This study examined the acid base disturbances in 18 adults with acute renal failure (ARF) from one of new aspects, which is lactate metabolism and pathophysiology. 10 patients (55%) of them were accompanied by lactic acidosis and 9 patients (90%) of those with lactic acidosis also had severe hepatic failure. Mortality of patients with lactic acidosis was 80%, and much higher than that of ARF (66.7%). Lactate, pyruvate, lactate-to-pyruvate ratio (L/P) were 76.7 +/- 15.66 mg/dl, 3.30 +/- 0.74 mg/dl and 19.9 +/- 1.41, respectively. All of them significantly raised, compared to values of healthy adults, patients with liver cirrhosis, chronic renal failure and diabetes mellitus. Arterial pH and HCO3- levels were 7.20 +/- 0.04 and 10.6 +/- 1.20 mEq/l. Anion gap (AG) was 30.0 +/- 3.66 mEq/l. Significant correlations of lactate with pH, HCO3-, AG and L/P were demonstrated, while correlations of lactate with BUN, CR and prothrombin time were not significantly observed. Lactic acidosis results from two mechanisms. One is lactate overproduction (e.g tissue hypoxia) and the other is lactate underutilization (e.g severe liver and/or renal failure). Whenever lactic acidosis occurred, both mechanisms were present simultaneously and continuously. Especially, the latter mechanism had a very important role on it, and seemed to decide the prognosis of the patients with lactic acidosis. Therapy of lactic acidosis was very difficult. First of all, we tried to improve the circulatory failure and severe acidemia (pH less than 7.20) not to fall into vicious cycle. Then, CAVH, if combined with alkali infusion, seemed to be the most useful technique in managing lactic acidosis with ARF.
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PMID:[Acute renal failure with lactic acidosis]. 221 21

Serum insulin-like growth factor (IGF) and IGF-binding protein (IGF BP) levels were determined in 13 insulin-dependent diabetic patients (30-60 yr of age) during an episode of severe metabolic decompensation and the recovery phase. After separation by acidic gel filtration, the samples were assayed for IGF using a protein-binding assay (which measures mainly IGF I-related peptides) and for IGF BP by measuring the binding activity, in both assays using IGF I as tracer. The reference standard was a pool of normal adult serum with an assigned potency of 1 U IGF and 1 U IGF BP per ml. The mean IGF level in the uncontrolled state, 0.55 +/- 0.05 (SEM) U/ml, was about half that of normal subjects (1.03 +/- 0.03 U/ml, P less than 0.001). With treatment, IGF levels reached the normal range within 3 days. The pattern of changes in IGF BP levels was roughly similar, although the values in the uncontrolled state were less depressed (0.78 +/- 0.04 U/ml vs. 0.98 +/- 0.04 in normal subjects, P less than 0.01). Highly significant correlations (P less than 0.001) were found between IGF levels and the biological parameters reflecting control of the diabetes: glycosuria (r = -0.60), glycemia (r = -0.52), ketonemia (r = -0.65), and HCO3- (r = 0.58). Similar but less significant correlations were found for IGF BP. The mean GH level during the period of metabolic decompensation (9.0 +/- 1.5 ng/ml) was elevated compared to that after recovery (2.9 +/- 0.8 ng/ml) (P less than 0.025). There was a negative correlation between GH values and IGF levels (r = -0.67, P less than 0.001). The correlation with IGF BP was much less significant (r = -0.38, P less than 0.05). The results clearly reflect the role of insulin and nutritional factors in the control of IGF levels. They also support the notion that the biosynthesis of IGF and IGF BP is not regulated in the same way.
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PMID:Serum levels of insulin-like growth factor (IGF) and IGF binding protein in insulin-dependent diabetics during an episode of severe metabolic decompensation and the recovery phase. 257 89

The studied group comprised 47 women in the 3rd trimester of pregnancy (29-40 weeks), including 17 with type I diabetes (study group) and 30 healthy women (control group). In the study group in one case diabetes was diagnosed during pregnancy and treated with diet only, in the remaining 16 pregnant women the mean diabetes duration was 6.2 years and the mean daily insulin dose was 70 u. According to White's classification one patient was in class A, 10 in class B and 6 in class C. In all cases renal function was normal, with normal blood values of creatinine, urea, electrolytes, uric acid, protein and acid-base equilibrium. Endogenous creatinine clearance was also normal. The studied biochemical parameters of renal tubular function included: 1) deamination of amino acids--with measurement of ammonium ion (NH4+) excretion with urine, 2) carbonic acid metabolism--with determination of urinary excretion of hydrogen ions (H+), 3) urinary excretion of sodium (Na+) and potassium (K+) ions. Besides that 24-hour urine was always measured. The studied women were similarly hydrated (standard diet, fluid balance control). The results were subjected to statistical analysis. In women with type I diabetes the volume of 24-hour urine was increased, although it fell within the normal range, urinary excretion of Na+ and K+ was raised. No change was found in amino-acid deamination an carbonic acid metabolism since the excretion of NH4+ and H+ was normal.
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PMID:[Various biochemical parameters of renal tubular function in patients with type I diabetes in the third trimester of pregnancy]. 270 87


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