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At least 1,207 records · Page 67Linked to original sources
PubMed2002

Accumulation of somatic mutation in mitochondrial DNA extracted from peripheral blood cells in diabetic patients.

AIMS/HYPOTHESIS: A point mutation of mitochondrial DNA at nucleotide number 3243 A to G is responsible for both the major genetic aetiologies of the MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) and mitochondrial diabetes. Otherwise, this mutation is also reported to occur as an acquired somatic mutation, possibly due to oxidative stress. Since diabetes can cause severe oxidative stress, we hypothesize that the accumulation of the somatic 3243 A to G mutation in mitochondrial DNA can be accelerated by diabetes. METHODS: DNA was extracted from blood samples of 290 non-diabetic healthy subjects (age 20-60) including 98 newborn infants and from 383 patients with Type II (non-insulin-dependent) diabetes mellitus (age 18-80). The extent of somatic 3243 A to G mutation to total mitochondrial DNA was detected by real-time PCR using the TaqMan Probe. RESULTS: Whereas the level of the 3243 A to G mutation was negligible in the newborn group, it was increased in healthy subjects who were 20 to 29 and 41 to 60 years of age, suggesting that this mutation was somatic. In the diabetic patients the mutation rate increased along with age and the duration of diabetes. In the middle-aged group (age 41-60), the 3243 A to G mutation accumulates fourfold higher in the diabetic patients than the healthy subjects. Moreover, multiple regression analysis showed that the most critical factor associated with this mutation in diabetic patients was the duration of diabetes. CONCLUSION/INTERPRETATION: Diabetes accelerates the accumulation of the somatic 3243 A to G mutation in mitochondrial DNA, which can accelerate the ageing process. This somatic mutation could possibly be a new marker for estimating the duration of diabetes.

Adenine↗
PubMed1988

Outpatient management of diabetic ketoacidosis.

An analysis of 63 pediatric diabetic patient visits to an emergency department for diabetic ketoacidosis was performed. Of 27 patients with a serum pH less than 7.20 or bicarbonate concentration less than 10 mmol/L (10 mEq/L) at admission, 25 (92%) had persistence of metabolic acidosis after three hours of outpatient therapy and were hospitalized. Of 36 patients with a serum pH greater than or equal to 7.20 or a bicarbonate concentration greater than or equal to 10 mmol/L (10 mEq/L) at admission, 34 (94%) had resolution of metabolic acidosis within three hours of initiating outpatient therapy and were discharged from the emergency department. The relapse rate in each group was similar. The initial serum glucose concentration accurately predicted duration of therapy necessary to resolve metabolic acidosis in the majority of patients discharged. Certain diabetic children can be treated for diabetic ketoacidosis with therapy administered in an outpatient setting. Most patients with an initial serum pH of 7.20 or higher or a bicarbonate concentration of 10 mmol/L (10 mEq/L) or higher will experience resolution of acidosis and tolerate feeding within three hours of initiating treatment.

Adolescent↗
PubMedDate not supplied

Medical care patterns at the onset of insulin-dependent diabetes mellitus: association with severity and subsequent complications.

The hospitalization of a child at the onset of insulin-dependent diabetes mellitus (IDDM) has become routine in many parts of the world, although controversy exists about its necessity. We examined the patterns of medical care use and the prognosis for acute complications after diagnosis for children with newly diagnosed IDDM in Colorado from 1978 to 1982. We reasoned that if children cared for entirely in outpatient settings at diagnosis had no more frequent acute complications after diagnosis than hospitalized children, we would be encouraged to further explore other potential benefits of outpatient care at onset. Twelve percent of 305 children studied statewide received only outpatient care during the first 2 wk after diagnosis, and, prognostically, their subsequent hospitalization and ketoacidosis rates were 2-3.7 times lower than those of children who received any inpatient care. No differences were noted for severe insulin reaction rates. Children classified as "severe" at onset, or with parents of lower education and income, or aged 10-14 yr at onset, regardless of care setting, had 2-4 times higher subsequent acute complication rates after onset than children without these characteristics. These findings, together with data on nights hospitalized and average length of stay in hospital at onset, suggest that a 42% reduction in total nights hospitalized could occur if children with "mild" or "normal" severity at onset were treated largely in the outpatient setting.

Acidosis↗
PubMed2006

The anion gap (AG): studies in the nephrotic syndrome and diabetic ketoacidosis (DKA).

Although "unmeasured" anions contribute to metabolic acidosis in a variety of disease states, they are generally not measured directly but estimated from the calculation of "gaps." Among the most commonly used method, the anion gap (AG) is not only a function of "unmeasured" anions, but also it is a function of plasma non-carbonate buffers (albumin and phosphate), the plasma pH, and the method of measurement. To clarify the contribution of non-carbonate buffers to the AG, the Figge-Fencl-Waston model of human plasma was applied to laboratory values obtained from two novel populations, patients with nephrotic syndrome and patients with diabetic ketoacidosis (DKA). The model performed adequately, justifying the common clinical practice of correcting the AG for the net protein charge.

Acetoacetates↗
PubMed1994

Pancreatic beta-cell secretory defect associated with mitochondrial point mutation of the tRNA(LEU(UUR)) gene: a study in seven families with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS).

Recent evidence suggests possible linkage between diabetes mellitus and mitochondrial gene mutation. We surveyed mitochondrial tRNA(LEU(UUR)) (3243) mutation in 7 mitochondrial encephalomyopathy, lactic acidosis and stroke-like episode (MELAS) families and identified 24 mutated subjects (7 MELAS probands and 17 non-MELAS relatives) as well as 11 non-mutant family members. An OGTT in the 24 mutant relatives revealed 14 diabetic subjects, 3 with impaired glucose tolerance and 7 with normal glucose tolerance and all non-mutant family members as having normal glucose tolerance. Insulinogenic index was significantly reduced in the mutant diabetic subjects and those with impaired and normal glucose tolerance in comparison with the normal control subjects and the non-mutant members. Urinary 24-h C-peptide immunoreactivity excretion was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance, compared with the control subjects and the non-mutant family members. Plasma C-peptide immunoreactivity 6 min after glucagon injection was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance compared with the control subjects and the non-mutant family members. Si, an index of insulin sensitivity of the four mutant subjects was within normal range. Islet cell antibodies were negative in sera of eight mutated diabetic subjects, 2 and 6 with impaired and normal glucose tolerance, respectively. Diabetic retinopathy and nephropathy were demonstrated in 7 (50%) and 12 (85.7%) of 14 mutant diabetic subjects, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1978

Diabetic ketoacidosis: new concepts and trends in pathogenesis and treatment.

New concepts concerning the pathogenesis and therapy of diabetic ketoacidosis are reviewed. The regulation of ketogenesis by intrahepatic enzymic processes and the roles of insulin deficiency or glucagon or other counterregulatory hormone excess are summarized. Major emphasis is placed on an analysis of the use of low-dose insulin regimens for the treatment of ketoacidosis. Most patients with diabetic ketoacidosis will respond to low-dose, hourly, intravenous or intramuscular regular insulin. Low doses of insulin are as effective as high doses and have fewer associated complications of hypoglycemia and hypokalemia. Phosphorus deficiency is common in diabetic ketoacidosis and hypophosphatemia usually becomes manifest within 4 to 12 h of institution of therapy. Phosphorus supplementation is now generally recommended to replete erythrocyte 2,3-diphosphoglycerate and improve oxygen delivery to tissues. Coexistent and biochemically significant lactic acidosis is a relatively infrequent complication of diabetic ketoacidosis and when present is usually due to underlying disorders associated with poor tissue perfusion.

Acetoacetates↗
PubMed2002

The acute effects of glycemic control on axonal excitability in human diabetic nerves.

OBJECTIVE: To investigate whether glycemic control is associated with reversible changes in axonal excitability in human diabetic nerves. It is known that voluntary contraction or compression ischemia alters nerve Na+/K+ pump activity, and axonal excitability changes due to the pump activity can be estimated by threshold tracking. METHODS: Threshold, the current required to produce a compound muscle action potential 50% of maximum, was determined from the stimulus-response curve, and threshold changes produced by maximal voluntary contraction or ischemia were measured before and after insulin treatment in 10 diabetic patients. RESULTS: Within 3 weeks of the start of treatment, the threshold changes became greater following voluntary contractions (+13+/-4% versus +23+/-5%; mean+/-SEM; p=0.04) and during ischemia (-5+/-2% versus -11+/-2%; p=0.04). CONCLUSIONS: The extent of threshold fluctuation depends on multiple metabolic factors associated with diabetes such as decreased Na+/K+ ATPase activity, increased anaerobic glycolysis, and tissue acidosis, and nerve excitability can respond quickly to glycemic control in diabetic patients.

Action Potentials↗
PubMed1984

Reversible pupillary miosis during a hyperglycaemic episode: case report.

A young female patient presented with non-ketotic hyperglycaemia, pupillary miosis and clouding of consciousness. The initial blood glucose was 83.3 mmol/l; there was no metabolic acidosis. After insulin therapy and improved diabetic control, pupillary function returned to normal. There was no other associated somatic or autonomic nerve dysfunction.

Adult↗
PubMed1977

Lactic acidosis.

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Acetates↗