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PubMed2003

A review of cochlear implantation in mitochondrial sensorineural hearing loss.

OBJECTIVE: Mitochondrial sensorineural hearing loss (SNHL) may be nonsyndromic (occurring in isolation), associated with the A1555G mutation in the MTRNR1 gene. Mitochondrial SNHL may also be syndromic, associated with the A3243G point mutation in the MTTL1 gene. In syndromic cases-mitochondrial encephalopathy, lactic acidosis, and strokelike episodes (MELAS), maternally inherited diabetes and deafness, Kearns-Sayre syndrome, and chronic progressive external ophthalmoplegia-the SNHL compounds already existing disabilities. The genetic basis for mitochondrial SNHL and postulated sites of pathologic changes are discussed. DATA SOURCES: Sources used were relevant clinical and basic science publications. STUDY SELECTION: A search of the entire databases of Medline and Web of Science, using various subject headings and free-text terms, was used to identify patients with mitochondrial disease having cochlear implants. DATA EXTRACTION: The data from publications were critically reviewed and tabulated to assess implantation outcomes. DATA SYNTHESIS: The data were not amenable to formal meta-analysis or valid data summarization, other than descriptive statistics. CONCLUSIONS: There is an increasing awareness of the prevalence of mitochondrial SNHL and its progressive nature. High-risk candidates warrant genetic testing and family screening. Correlating the data for mitochondrial SNHL as a treatable entity is important, and the authors present an overview of these patients successfully rehabilitated by cochlear implantation.

Adult↗
PubMed2004

High-sensitivity detection of the A3243G mutation of mitochondrial DNA by a combination of allele-specific PCR and peptide nucleic acid-directed PCR clamping.

BACKGROUND: The A3243G mutation of mitochondrial DNA (mtDNA) is involved in many common diseases, including diabetes mellitus and mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS). For detection of this mutation, allele-specific PCR is highly sensitive but requires strict control of PCR conditions; it thus is not adequate for a routine clinical test. We aimed to develop a routinely available PCR method for quantitative detection of low-level heteroplasmy of the A3243G mutation. METHODS: Quantitative allele-specific PCR for the A3243G mutation was performed in the presence of peptide nucleic acid (PNA), in which PNA is complementary to the wild-type mtDNA, with one primer having a 3' end matched to nucleotide position 3243 of the mutant. RESULTS: With our method, amplification of wild-type mtDNA was suppressed 7000-fold compared with amplification of the mutant mtDNA under a broad range of conditions: DNA, 5-100 ng; annealing temperature, 61-66 degrees C; and PNA, 1.5-3.5 micromol/L. Hence, 0.1% heteroplasmy of the A3243G mutation can be reliably quantified by this method. Blood samples form 40 healthy volunteers showed <0.06% heteroplasmy, suggesting that 0.1% is diagnostically significant. CONCLUSIONS: PNA maintains the specificity of allele-specific PCR over a wide range of conditions, which is important for routine clinical testing.

Alleles↗
PubMed1998

Glutamine, exercise and immune function. Links and possible mechanisms.

Glutamine is the most abundant free amino acid in human muscle and plasma and is utilised at high rates by rapidly dividing cells, including leucocytes, to provide energy and optimal conditions for nucleotide biosynthesis. As such, it is considered to be essential for proper immune function. During various catabolic states including surgical trauma, infection, starvation and prolonged exercise, glutamine homeostasis is placed under stress. Falls in the plasma glutamine level (normal range 500 to 750 mumol/L after an overnight fast) have been reported following endurance events and prolonged exercise. These levels remain unchanged or temporarily elevated after short term, high intensity exercise. Plasma glutamine has also been reported to fall in patients with untreated diabetes mellitus, in diet-induced metabolic acidosis and in the recovery period following high intensity intermittent exercise. Common factors among all these stress states are rises in the plasma concentrations of cortisol and glucagon and an increased tissue requirement for glutamine for gluconeogenesis. It is suggested that increased gluconeogenesis and associated increases in hepatic, gut and renal glutamine uptake account for the depletion of plasma glutamine in catabolic stress states, including prolonged exercise. The short term effects of exercise on the plasma glutamine level may be cumulative, since heavy training has been shown to result in low plasma glutamine levels (< 500 mumol/L) requiring long periods of recovery. Furthermore, athletes experiencing discomfort from the overtraining syndrome exhibit lower resting levels of plasma glutamine than active healthy controls. Therefore, physical activity directly affects the availability of glutamine to the leucocytes and thus may influence immune function. The utility of plasma glutamine level as a marker of overtraining has recently been highlighted, but a consensus has not yet been reached concerning the best method of determining the level. Since injury, infection, nutritional status and acute exercise can all influence plasma glutamine level, these factors must be controlled and/or taken into consideration if plasma glutamine is to prove a useful marker of impending overtraining.

Animals↗
PubMed1999

A risk-benefit assessment of metformin in type 2 diabetes mellitus.

Metformin has been used for over 40 years as an effective glucose-lowering agent in type 2 (noninsulin-dependent) diabetes mellitus. Typically it reduces basal and postprandial hyperglycaemia by about 25% in more than 90% of patients when either given alone or coadministered with other therapies including insulin during a programme of managed care. Metformin counters insulin resistance and offers benefits against many features of the insulin resistance syndrome (Syndrome X) by preventing bodyweight gain, reducing hyperinsulinaemia and improving the lipid profile. In contrast to sulphonylureas, metformin does not increase insulin secretion or cause serious hypoglycaemia. Treatment of type 2 diabetes mellitus with metformin from diagnosis also offers greater protection against the chronic vascular complications of type 2 diabetes mellitus. The most serious complication associated with metformin is lactic acidosis which has an incidence of about 0.03 cases per 1000 patients years of treatment and a mortality risk of about 0.015 per 1000 patient-years. Most cases occur in patients who are wrongly prescribed the drug, particularly patients with impaired renal function (e.g. serum creatinine level > 130 micromol/L or > 1.5 g/L). Other major contraindications include congestive heart failure, hypoxic states and advanced liver disease. Serious adverse events with metformin are predictable rather than spontaneous and are potentially preventable if the prescribing guidelines are respected. Gastrointestinal adverse effects, notably diarrhoea, occur in less than 20% of patients and remit when the dosage is reduced. The life-threatening risks associated with metformin are rare and could mostly be avoided by strict adherence to the prescribing guidelines. Given the 4 decades of clinical experience with metformin, its antihyperglycaemic efficacy and benefits against Syndrome X, metformin offers a very favourable risk-benefit assessment when compared with the chronic morbidity and premature mortality among patients with type 2 diabetes mellitus.

Acidosis, Lactic↗
PubMedDate not supplied

[Use of biguanide preparations in the treatment of diabetes mellitus].

The blood content of lactic acid was measured in 186 patients with overt diabetes mellitus. The patients had normal or excess body weight and were placed on different treatment methods during decompensation, subcompensation and compensation stages. During diabetes mellitus compensation attained with different treatment methods as well as during treatment including biguanides in the presence of normoglycemia, the mean blood level of lactic acid did not differ significantly from its mean content in normal subjects. Patients with decompensated diabetes mellitus manifested a significant elevation of the mean blood content of lactic acid. There was a definite relationship between the glycemia and high lactic acid level in the blood. Based on an analysis of the reported data and own materials the conclusion is drawn that biguanides should not be used in the treatment of decompensated diabetes mellitus, since this may lead to an increase in blood lactic acid and to the growth of lactic acidosis risk. It is proposed that contraindications to the use of biguanides in diabetes mellitus patients should also include hyperglycemia. Indications to the use of biguanides in diabetes mellitus patients are provided as well as the table of diseases in which biguanides are contraindicated. A list of drugs incompatible with biguanides is also presented. It is recommended that biguanides should not be applied for over 4 to 6 months. It is also recommended that detection of blood lactic acid should be introduced into medical practice on a wider basis, since lactic acidosis cannot be diagnosed without using such a test.

Adolescent↗
PubMedDate not supplied

Recovery from decompensated non-insulin-dependent diabetes mellitus: studies of C-peptide secretion.

Eleven non-insulin-dependent diabetic patients presented with decompensated hyperglycemia. Nine had pronounced ketonuria, five with acidosis. In seven cases, precipitating factors were identified. In the other four cases, including three cases of diabetic ketoacidosis, no identifiable triggering events were present. In each case, recovery from the initially decompensated diabetic state occurred. Eventually, all patients were managed by diet alone. Seven patients demonstrated nondiabetic glucose tolerance tests (GTT). Several patients underwent stressful situations after "recovery" without recurrence of hyperglycemia. Glucose-stimulated C-peptide levels were determined postrecovery. C-peptide secretion was in the normal range and, in fact, was identical, in relation to glucose levels, to that in a group of nondiabetic volunteers. In 6 of the 11 cases, C-peptide secretion was measured at the time of initial presentation. These levels were markedly lower than comparable values during the GTT postrecovery. Non-insulin-dependent diabetes, even when presenting in a decompensated state, is subject to a considerable degree of reversibility and even recovery to a nondiabetic state in some cases. Recovery is associated with a return to normal C-peptide secretion.

Adult↗
PubMed2001

Olanzapine-associated severe hyperglycemia, ketonuria, and acidosis: case report and review of literature.

Olanzapine has been associated with insulin resistance and new-onset diabetes mellitus. A 27-year-old African-American man developed new-onset severe hyperglycemia-glucose 1240 mg/dl, with ketonuria and acidosis, but no weight gain-2 years after starting olanzapine. Although his diabetes was stabilized with insulin, his family had difficulty monitoring his therapy, and insulin was discontinued. Subsequent monotherapy with pioglitazone stabilized the patient's glucose levels, allowing him to continue taking olanzapine. Health care professionals should be aware of links between olanzapine and diabetes mellitus and of the potential for delayed recognition of complications associated with diabetes in patients who are psychotic. Insulin poses additional problems because families of patients with schizophrenia have to deal with compliance and risk of accidental or suicidal overdose. This case and others described in the literature illustrate such dilemmas and highlight the need to further study links connecting diabetes, insulin resistance, and olanzapine. Further research to determine proportionality and risk differences among various atypical antipsychotics also is warranted.

Adult↗
PubMed1994

Stroke in the diabetic patient.

A higher prevalence of stroke is found in the patient with both diagnosed and undiagnosed diabetes and glucose intolerance. Because of local cerebral acidosis caused by ischemia and hyperglycemia, morbidity and mortality from a stroke are increased. Most studies show that individuals with admission serum glucose > 120 mg/dl (6.7 mM) have a higher morbidity and mortality from a stroke. The prevalence of cerebral infarcts, especially lacunar infarcts, is increased and the prevalence of subarachnoid hemorrhage, cerebral hemorrhage, and transient ischemic attacks are decreased in the diabetic patient. Age, race, hypertension, and the presence of diabetic nephropathy and coronary and peripheral vascular disease are risk factors for stroke in the diabetic patient, whereas obesity, smoking, hyperlipidemia, and glycemic control are not. Investigation and treatment of the diabetic patient with a stroke is discussed.

Cerebrovascular Disorders↗
PubMed1998

Glucose metabolism, H+ production and Na+/H+-exchanger mRNA levels in ischemic hearts from diabetic rats.

Glycolysis uncoupled from glucose oxidation is a major reason for the intracellular acidosis that occurs during severe myocardial ischemia. The imbalance between glycolysis and glucose oxidation, and the resultant H+ produced from glycolytically derived ATP hydrolysis in the diabetic rat heart is the focus of this study. Isolated working hearts from 6 week streptozotocin diabetic rat hearts were perfused with 11 mM glucose and 1.2 mM palmitate and subjected to a 25 min period of global ischemia. A second series of experiments were also performed in which hearts from control, diabetic, and islet-transplanted diabetic rats were subjected to a 30 min aerobic perfusion, followed by a 60 min period of low-flow ischemia (coronary flow = 0.5 ml/min) and 30 min of aerobic reperfusion. H+ production from glucose metabolism was measured throughout the two protocols by simultaneous measurement of glycolysis and glucose oxidation using perfusate labelled with [5-3H/U-14C]-glucose. Rates of H+ production were calculated by measuring the difference between glycolysis and glucose oxidation. The H+ production throughout the perfusion was generally lower in diabetic rat hearts compared to control hearts, while islet-transplantation of diabetic rats increased H+ production to rates similar to those seen in control hearts. This occurred primarily due to a dramatic increase in the rates of glycolysis. Despite the difference in H+ production between control, diabetic and islet-transplanted diabetic rat hearts, no difference in mRNA levels of the cardiac Na+/H+-exchanger (NHE-1) was seen. This suggests that alterations in the source of protons (i.e. glucose metabolism) are as important as alterations in the fate of protons, when considering diabetes-induced changes in cellular pH. Furthermore, our data suggests that alterations in Na+/H+-exchange activity in the diabetic rat heart occur at a post-translational level, possibly due to direct alterations in the sarcolemmal membranes.

Animals↗
PubMed1995

A subtype of diabetes mellitus associated with a mutation in the mitochondrial gene.

Recently, in patients with diabetes and deafness, researchers have identified an A to G transition at position 3243 in transfer ribonucleic acid(Leu)(UUR) [3243 base-pair (bp) mutation], originally found in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes. To determine the prevalence of diabetic patients with this mutation in Japan, we screened selected cohorts of diabetic patients based upon type of diabetes, family history of diabetes, and age of onset; also screened were 550 unselected cohorts of diabetic patients, without prior information. We identified 5 patients with the 3243-bp mutation, suggesting that approximately 0.9% of diabetic patients have it. However, there were none with this mutation in 250 controls with normal glucose tolerance. We also studied the clinical characteristics and insulin secretory characteristics of diabetic patients with 3243-bp mutation. We propose that diabetes mellitus with 3243-bp mutation is a novel subtype of diabetes mellitus, maternally inherited diabetes, and deafness (MIDD).

Adult↗
PubMed2003

Treatment of diabetic ketoacidosis in children and adolescents.

Diabetic ketoacidosis (DKA) may be defined as a metabolic derangement characterized by hyperglycemia, acidosis and ketonuria. It is a crucial pediatric medical emergency. DKA may occur in children with diabetes at onset due to severe insulin deficiency, in established patients from failing to take insulin, acute stress, and poor sick-day management. The treatment of DKA has undergone a radical transformation over recent years. Among the major innovations the early adjustment of the hydroelectrolyte imbalance and the continuous i.v. infusion of microdoses of insulin are the most interesting. Despite appropriate use of insulin and fluids, and continuous clinical observation, the mortality rate has not improved, and has remained the same as that reported in the 1970s. DKA can be prevented by shortening the period of carbohydrate intolerance that usually precedes the diagnosis of Type 1 diabetes. Its prevention decreases morbidity and mortality and allows to save on the hospital costs. The aim of this paper is to review the main aspects of the treatment and prevention of DKA.

Adolescent↗
PubMed1983

[Continuous subcutaneous insulin infusion: long-term treatment in an unselected group of insulin-dependent diabetics].

Long-term ambulatory continuous subcutaneous insulin infusion was undertaken under serial blood-glucose control in nine insulin-dependent diabetics. Before this treatment was started, haemoglobin A1 was increased (more than 13%), diabetic lipoid necrosis was present in three, proliferative diabetic retinopathy in one, treatment-resistant Candida oesophagitis in one and Addison's disease in one. During the total of 630 weeks (range 6-135 weeks) of continuous subcutaneous insulin infusion it was found that (1) the metabolic state of the patients improved significantly, the previously non-responding oesophagitis healed and one of three patients with diabetic lipoid necrosis was markedly improved; (2) the risks of insulin treatment, hypoglycaemia (especially with Addison's disease) and keto-acidosis (for technical reasons) remained; and (3) in long-standing diabetes of type I even good control of blood glucose levels (mean 113 mg/dl) could neither prevent the occurrence of proliferative diabetic retinopathy nor loss of sight.

Adult↗
PubMed1992

Regulation of phosphoenolpyruvate carboxykinase mRNA in mouse liver, kidney, and fat tissues by fasting, diabetes, and insulin.

Previous investigations of the phosphoenolpyruvate carboxykinase (PEPCK) gene have been conducted using rats. In a recent comparative study, we investigated, for the first time, the effects of fasting, refeeding, alloxan-induced diabetes, and insulin treatment on the levels of PEPCK mRNA in mouse liver, kidney, and adipose tissues. As in rats, fasting and diabetes induced, while insulin repressed, hepatic PEPCK mRNA. In contrast, the response of renal PEPCK mRNA to fasting, refeeding, and diabetes in mice differed quantitatively with that in rats: fasting caused a twofold increase in mice and a fourfold increase in rats. Moreover, diabetes, which induces renal PEPCK mRNA indirectly by causing acidosis in rats, was without effect in mice. In adipose tissue, the results of previous studies in both rats and mice have shown that the amount of PEPCK protein and its rate of synthesis are increased by fasting and diabetes and decreased by refeeding and insulin treatment. Thus, it was surprising to find that fasting, refeeding, alloxan-induced diabetes, and insulin treatment had no effect on adipose tissue PEPCK mRNA in either rats or mice.

Adipose Tissue↗