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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The isolated perfused rat pancreas was used to investigate how adrenergic influences within the pancreas might mediate ammonia-induced glucagon secretion. The addition of 2 mM ammonia to the perfusate increased norepinephrine release and glucagon secretion in the effluent. Upon cessation of ammonia addition, a pronounced burst of glucagon release was observed. Alpha-adrenergic blockade with phentolamine (10 microM) blocked the glucagon response to ammonia. Beta-adrenergic blockade with propranolol (10 microM) had no significant effect on the amount of glucagon release induced by ammonia. Depletion of norepinephrine from sympathetic nerve terminals by pretreatment with 6-hydroxydopamine lowered the pancreatic norepinephrine content to less than 16% of the control value and diminished the glucagon and norepinephrine response to ammonia almost completely. The burst of glucagon release after the removal of ammonia was inhibited to 2% of the control value by phentolamine and to 57% by propranolol. Pretreatment with 6-hydroxydopamine reduced the burst of glucagon secretion to 28% of the control value. Neither phentolamine nor propranolol reduced the magnitude of the ammonia-induced suppression of insulin secretion. We conclude that the effect of ammonia on glucagon release from the isolated rat pancreas is mediated by intrapancreatic adrenergic control.
Diabetes Res Clin Pract 1988 Sep 05
PMID:Adrenergic control of the glucagon response to ammonia in the perfused rat pancreas. 314 94

Eighteen women with insulin-dependent diabetes mellitus (IDDM) and 15 nondiabetic women participated in a study of the relationship of zincuria to measures of glycemic control, renal function, and tissue catabolism. In the IDDM women, mean +/- SE glycosylated hemoglobin was 9.8 +/- 0.5%, and fasting plasma glucose was 189 +/- 19 mg/dl; duration of diabetes averaged 15 yr. In comparison with control women, the IDDM women excreted four times as much zinc in the urine. However, the total plasma zinc concentration was significantly higher in the IDDM than in the control women (14.7 vs. 13.4 microM). The increased urinary zinc loss in the IDDM women was not related to urine volume, urinary glucose excretion, fasting plasma glucose concentration, percent glycosylated hemoglobin, or an increased glomerular filtration rate. Total urinary protein losses were four times higher in the IDDM women than in the control women, and these urinary protein losses correlated with the urinary zinc losses (P less than .007). There was no relationship between urinary zinc and the excretion of any of the amino acids, urea, or ammonia. The results of this study show that hyperzincuria in diabetes is not associated with lower plasma zinc levels. An increased zinc absorption, decreased intestinal zinc excretion, or increased tissue catabolism may support higher plasma zinc levels.
Diabetes Care
PMID:Hyperzincuria in IDDM women. Relationship to measures of glycemic control, renal function, and tissue catabolism. 324 98

A simple and reliable method is described which is suitable for estimation of a whole blood phenylalanine concentration for the patient with PKU in various settings including the physician's office and the home. Excellent correlations were obtained between this method and weighed phenylalanine standards, as well as with measurement of phenylalanine in serum, plasma, and whole blood, using the McCaman-Robins fluorometric assay. Increasing the frequency and rapidity of feedback to the patient should improve metabolic control, just as home glucose monitoring has for the patient with diabetes mellitus. This method is immediately adaptable to monitoring patients with tyrosinemia, and with substitution of the appropriate amino acid ammonia lyase could be used for other amino acidemias.
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PMID:Blood phenylalanine estimation for the patient with phenylketonuria using a portable device. 335 20

Effects of ammonia on glucagon and insulin secretion from the perfused pancreas of cirrhotic rats were investigated to clarify the occurring mechanism of hypersecretion of pancreatic glucagon in liver cirrhotics. The results were as follows: During ammonia loading, insulin secretion was inhibited in a dose-related manner, whereas glucagon secretion was gradually increased at high concentrations of ammonia (2 mM) in control rats; this tendency was augmented in the presence of alpha-ketoglutarate in cirrhotic rats. On cessation of ammonia loading, a transient but definite increase in glucagon and insulin secretion was observed. Basal plasma glucagon and ammonia levels as well as basal glucagon secretion from the perfused pancreas of cirrhotic rats were significantly higher than in control rats. Basal insulin secretion from the perfused pancreas of cirrhotic rats was not different in spite of high levels of plasma insulin. Glucagon secretory response to glucose and arginine from the perfused pancreas of cirrhotic rats was higher than in the control pancreas, whereas insulin secretion was lower. In these cirrhotic rats, an increase in the number of islet cells, particularly A cells, was observed. These data suggested that hypersecretion of pancreatic glucagon which was responsible for hyperglucagonemia in cirrhotic rats might be attributed to high levels of ammonia and alpha-ketoglutarate in blood as well as to the fluctuation of abnormal ammonia concentration in blood and to the hypertrophy of islets, particularly of the A cell group due to hypersecretion.
Diabetes Res Clin Pract 1986 Jun
PMID:Effect of ammonia on glucagon secretion from the perfused pancreas of cirrhotic rats. 352 23

The effect of alloxan diabetes on citrulline formation from NH4Cl and bicarbonate was studied in rabbit liver mitochondria incubated with glutamate or succinate as respiratory substrate, as well as with exogenous ATP in the presence of uncoupler and oligomycin. In contrast to ornithine transcarbamoylase, the activity of carbamoyl-phosphate synthetase (ammonia) was higher in mitochondria from diabetic animals than in those from normal ones. In diabetic rabbits the rates of citrulline synthesis were stimulated under all conditions studied. In contrast, levels of N-acetylglutamate, an activator of carbamoyl-phosphate synthetase (ammonia), were significantly increased only in the presence of glutamate, while the highest rates of citrulline formation occurred in uncoupled mitochondria incubated with exogenous ATP as energy source. Treatment of animals with alloxan resulted in an increase of both the intramitochondrial ATP level and the rate of adenine nucleotide translocation across the mitochondrial membrane. The results indicate that the stimulation of citrulline formation in liver mitochondria of diabetic rabbits is mainly due to an increase in carbamoyl-phosphate synthetase (ammonia) activity and an elevation of content of intramitochondrial ATP, a substrate of this enzyme.
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PMID:The stimulatory effect of alloxan diabetes on citrulline formation in rabbit liver mitochondria. 397 23

Normally the kidneys respond to an acid load by increased ammonia production. In six patients with adult-type diabetes this response was reduced by a mean 50% after a therapeutic dose of phenformin. The reduced ability to compensate for acid loads may be one factor leading to metabolic acidosis and lactoacidosis sometimes associated with phenformin therapy.
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PMID:Renal response to acid load after phenformin. 475 35

Proteins exposed to glucose over long periods are known to undergo physicochemical changes including crosslinking and formation of brown fluorescent pigments of poorly characterized structure. Acid hydrolysis of both browned poly(L-lysine) and browned bovine serum albumin is found to release a major fluorescent chromophore, which after alkalinization is extractable into organic solvents and which can be purified by silica gel chromatography. The fluorescence properties of this compound very closely resemble those of the bulk browned polypeptides. By NMR, mass spectroscopy, and chemical derivatization, this compound is assigned the structure 2-(2-furoyl)-4(5)-(2-furanyl)-1H-imidazole (FFI). Confirmation was obtained by independent chemical synthesis from furylglyoxal and ammonia. The incorporation of two peptide-derived amine nitrogens and two glucose residues in FFI strongly suggests that peptide-bound FFI precursors are implicated in the crosslinking of proteins by glucose in vivo. This reaction has potential implications in the understanding of glucose-mediated protein modifications and their role in the complications of diabetes and aging.
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PMID:Aging of proteins: isolation and identification of a fluorescent chromophore from the reaction of polypeptides with glucose. 658 21

Quantification of 2-ketoglutaric acid in plasma and cerebrospinal fluid as its O-trimethylsilyl++-quinoxalinol derivative by gas chromatography chemical ionization mass spectrometry is described with benzoylformic acid as internal standard. This technique, with ammonia as reactant gas, only detects the protonated molecular ions. The recovery of 2-ketoglutarate from perchloric-deproteinized plasma is 99.7 +/- 1.2%. The normal value of 2-ketoglutarate in children is 8.6 +/- 2.6 mumol l-1 (mean +/- standard deviation) in plasma (n = 25) and 4.8 +/- 1.4 mumol l-1 in cerebrospinal fluid (n = 20). The plasma level of 2-ketoglutarate is correlated with urea concentration (r = 0.96; p less than 0.001) in healthy subjects and in patients with chronic renal insufficiency. Increased values are found in one case of pyruvate carboxylase deficiency, and inconstantly in diabetes; physiological variations are described during fasting and after an oral glucose load.
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PMID:Microdetermination of 2-ketoglutaric acid in plasma and cerebrospinal fluid by capillary gas chromatography mass spectrometry; application to pediatrics. 670

Metabolic acidosis with a normal anion gap results from either bicarbonate loss or a urine acidification defect. The bicarbonate loss may be via the gastrointestinal tract or the urine, or may be indirect due to excretion of the sodium and potassium as opposed to the ammonium salts of ketone body anions. Defects in urine acidification in the diabetic have several etiologies: first, hydrogen ion secretion may be decreased because of an intrinsic defect in the hydrogen ion pump (i.e., diseases of the renal medulla); second, there may be a failure to augment hydrogen ion secretion by a favorable electrical gradient (e.g., reduced mineralocorticoids); and third, there may be a failure to generate a favorable chemical gradient to augment hydrogen ion secretion (e.g., reduced urine ammonia). Reduced levels of aldosterone associated with hyporeninemia has been termed type IV RTA, and these patients have specific therapeutic needs.
Diabetes 1981 Sep
PMID:Selected aspects of the pathophysiology of metabolic acidosis in diabetes mellitus. 679 Mar 25

Renal elimination of uric acid, calcium, phosphorus, sodium, potassium, chloride and magnesium and urinary acidification capacity were determined in ten insulin-dependent diabetics and in ten matched control subjects. The diabetics showed excessive excretion of uric acid, sodium, potassium, chloride and ammonia. Sodium, chloride and ammonia excretion fractions was also increased with respect to controls. The enhanced excretion of these substances in diabetics failed to relate to glomerular filtration rate, glycosuria or insulin requirements. These findings might be explained on the basis of glomerular filtration rate elevation, tubular response to this increment, and the underlying metabolic disturbances of diabetes.
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PMID:Renal tubular function and urinary acidification capacity in early juvenile diabetes. 730 70


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