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PubMed1996

Metabolic response of forearm muscle to graded exercise in type II diabetes mellitus: effect of endurance training.

In this study, 31P nuclear magnetic resonance spectroscopy was used to monitor muscle metabolism in Type II diabetic subjects (n = 10) during an incremental exercise test. Also the exercise responses of diabetic subjects (n = 4) following submaximal endurance training were assessed and compared to healthy controls (n = 5). Responses to incremental exercise in the diabetic subjects were consistent over time despite minor fluctuations in metabolic control. In the diabetic and control groups, after 12 weeks of training the forearm flexor muscles, power output at the intracellular threshold of acidosis (IT) increased (p < .01) similarly: T0 versus T12: 0.90 +/- 0.09 versus 1.20 +/- 0.13 and 1.03 +/- 0.07 versus 1.22 +/- 0.10 W, respectively. Minimum intracellular pH reached at peak exercise was unchanged after training. The control group, however, became more acidic versus the diabetic group (p < .05) in response to progressive exercise. This difference was maintained over time. Endurance training elicited similar adaptations in forearm muscles of Type II diabetic and control subjects, although there were differences between the two groups in intracellular pH during exercise.

Acidosis↗
PubMed2006

Reconciling diabetes management and the ketogenic diet in a child with pyruvate dehydrogenase deficiency.

A 4-year-old girl with pyruvate dehydrogenase deficiency, static encephalopathy, and seizure disorder treated with the ketogenic diet presented in severe diabetic ketoacidosis. Pyruvate dehydrogenase deficiency is a rare genetic defect of mitochondrial energy metabolism that leads to inefficient glucose use and lactic acidosis. The ketogenic diet provides the brain with an alternate fuel source, but its implementation opposes traditional diabetes management. Faced with this therapeutic dilemma, we aimed to maintain ketosis without compromising safety to optimize neurologic function and quality of life. This is the first report, to our knowledge, of a child simultaneously treated with the ketogenic diet and exogenous insulin. A 28-month follow-up revealed excellent glycemic control, improved activity level, significant developmental achievements, and, perhaps most striking, catch-up linear growth from < 5th percentile to the 50th percentile. Her progress to date indicates that diabetes does not preclude use of the ketogenic diet.

Child, Preschool↗
PubMed1978

The effects of phenformin in normal vs. diabetic isolated perfused rat liver.

In the isolated perfused liver system high concentrations of phenformin (0.93--1.24 mM) were required to reduce the greater than two-fold elevated rate of gluconeogenesis from L-[U-14C]lactate in acutely alloxan diabetic (48-hour) and chronically alloxan diabetic (7-day) rat livers to the slower rate of normal fed livers. At these phenformin concentrations, other hepatic functions such as substrate uptake and 14CO2 production were also inhibited. The livers were also in a very reduced state under these conditions as indicated by the elevated ratios of the redox couples lactate/pyruvate and 3-hydroxybutyrate/acetoacetic acid. The results are interpreted to indicate that if phenformin functions as an antidiabetic (hypoglycemic) agent by inhibiting hepatic gluconeogenesis to normal levels, it is also generally toxic to the liver under such conditions. The results are discussed in relation to current hypotheses of the mechanism of action of phenformin and to phenformin-associated lactic acidosis.

Animals↗
PubMed2000

Absence of maternal A3243G mtDNA mutation and reversible hyperglycemia in a patient with MELAS syndrome.

We report the unusual features of a female patient who had MELAS-specific A3243G mutation in mitochondrial DNA (mtDNA) and diabetes mellitus (DM). The patient showed mitochondrial myopathy, encephalopathy, lactic acidosis, and deafness but lacked the stroke-like episode. Acute hyperglycemia was noted after one attack of status epilepticus. Molecular genetic analysis demonstrated a heteroplasmic A3243G point mutation in the mtDNAs of muscle, blood cells and hair follicles. Glucagon stimulation test exhibited marked depression of pancreatic beta-cell function. However, in a further study neither this mutation, nor MELAS syndrome or DM, was found in all of her maternal relatives. A series of follow-up studies for beta-cell function also showed gradual improvement. The pedigree study led us to believe that this A3243G mutation arose from the germ line cells or occurred later in somatic tissues of the patient. We also suggest that the A3243G mutation of mtDNA may elicit the pathogenesis of a subtype of DM. Nevertheless, environmental stress may be another important factor for provocation of the disease.

Adult↗
PubMed2000

Effects of ketoacidosis on rat apolipoprotein A1 gene expression: a link with acidosis but not with ketones.

To determine if ketoacidosis contributes to reduced apolipoprotein A1 (apoA1) expression in insulin-deficient diabetic rats, we examined the regulation of apoA1 gene expression in response to changes in ambient pH or ketone body concentrations. Hepatic apoAI mRNA levels were reduced 42% in diabetic rats relative to nondiabetic controls (means+/-s.d.; 321.8+/-43.7 vs 438.7+/-58.8 arbitrary units; P<0.03). Neither endogenous apoA1 mRNA nor transcriptional activity of the rat apoA1 gene promoter (from -474 to -7) were altered by sodium butyrate or isobutyramide (0.3 mM to 10 mM) in Hep G2 or Caco-2 cells. Rat hepatic and intestinal apoA1 mRNA levels, and plasma apoA1 concentration, were not altered 24 h after isobutyramide administration (500 mg/kg by gavage). When the effect of altering ambient pH within a wide range commonly encountered in vivo was studied, acidosis (pH 6.7), relative to alkalosis (pH 7.9), decreased apoAI mRNA levels relative to glyceraldehyde-3-phosphate dehydrogenase mRNA by 47% in Hep G2 cells (P<0.025) and by 24% in Caco-2 cells (P<0.017). Acidosis did not alter cytomegalo virus (CMV)-beta-galactosidase activity, or the activity of the simian virus (SV40) early-region promoter, in either cell line transfected with the respective constructs. The lowering of ambient pH was associated with a graded reduction in apoAI promoter activity. At pH 6.7, apoAI promoter activity was reduced by 75% compared with promoter activity at pH 7.9. These observations indicate that acidosis, but not ketosis, contributes to the reduction in apoA1 expression during diabetic ketoacidosis by down-regulating apoAI promoter activity.

Amides↗
PubMed1999

Risk factors for developing brain herniation during diabetic ketoacidosis.

The charts were reviewed of children admitted in diabetic ketoacidosis (DKA) to one hospital within 12 years. The frequency of brain herniation after admission was nine of 153 children admitted for one or more episodes of DKA. The severity of acidosis and hypercapnea were the most reliable risk factors. None of the children who maintained a blood pH greater than 7.1 and a capillary blood partial pressure of carbon dioxide (PCO2) greater than 20 mm Hg manifested brain herniation. The rate of initial fluid administration in severe DKA was also a risk factor. Of 119 patients having a blood pH less than 7.1 or PCO2 less than 20 mm Hg, none of 32 receiving less than 25 mL/kg, one of 42 receiving 25-50 mL/kg, and eight of 40 receiving more than 50 mL/kg of intravenous fluid during the first (in Patient 9, the second) 4 hours of therapy sustained brain herniation. Equally dehydrated unaffected patients initially receiving 25-50 mL/kg/4 hours of intravenous fluid did not develop signs of hypovolemia or worsening DKA. In this series, hydrating at a rate greater than 50 mL/kg during the first 4 hours offered no advantage and was associated with an increased risk of brain herniation.

Acidosis↗
PubMed1991

Primary hyperparathyroidism and coexisting nephrogenic diabetes insipidus: rapid postoperative correction.

Shortly after diagnosis of primary hyperparathyroidism, a patient had serum hyperosmolality, polyuria, isosthenuria, profound potassium depletion, and elevated plasma antidiuretic hormone levels, all consistent with nephrogenic diabetes insipidus. After parathyroidectomy, serum calcium and serum osmolality levels fell concurrently. Profound potassium deficits did not recur. We propose that (1) hypercalcemia produced a concentrating defect and polyuria; (2) renal tubular acidosis and polyuria combined to produce severe potassium depletion; (3) hypokalemia potentiated the nephrogenic diabetes insipidus caused by hypercalcemia; and (4) postoperative disappearance of the diabetes insipidus confirmed its reversible, purely metabolic causes.

Diabetes Insipidus↗
PubMedDate not supplied

Epidemiology and treatment of diabetic ketoacidosis in a community population.

We evaluated the epidemiology of diabetic ketoacidosis in the period 1960-1979. In Frederiksborg County, Denmark, the incidence of ketoacidosis at the county hospital increased from 60 per 100,000 in the period 1943-1963 to 120 per 100,000 in the period 1960-1979. In the investigation period we found an increasing incidence confined to urban areas. Precipitating factors were not somatic in 53% of the cases. Patients in the lowest social class (V) were in a higher risk group, experiencing ketoacidosis more often and having a higher frequency of severe acidosis. Forty-nine percent of the patients have had a diabetes duration of more than 5 yr. The lethality rate decreased from the period 1943-1963 and was 4.7% in the investigation period 1960-1979.

Adolescent↗
PubMed1987

Relationship between renal function and metabolic alterations in early streptozocin-induced diabetes in rats.

To investigate the temporal relationship of diabetes-induced renal growth and its associated metabolic alterations to the early development of renal hyperfunction, parallel functional and metabolic studies were performed shortly after the onset of diabetes in rats. Hyperglycemia and hypoinsulinemia were evident 18 h after streptozocin injection, and significant hyperglucagonemia and acidosis were present at 36-48 h. Glomerular filtration rate (GFR), expressed per unit of body weight, first increased at 3 days of diabetes [1.35 +/- 0.07 (SE) (N = 14)] and was 18% greater than in controls [1.14 +/- 0.03 ml X min-1 X 100 g-1 (SE) (N = 38)] (P less than .005). Renal enlargement preceded GFR changes, so that GFR per unit of kidney weight was lower at 48 h in diabetics [1.31 +/- 0.06 (SE) (N = 16)] than in controls [1.54 +/- 0.04 ml X min-1 X g-1 (SE) (N = 38)] (P less than .01). Nucleotide and RNA metabolism was studied in the renal cortex after infusion of radio-labeled orotate or adenine. Rate of RNA synthesis, total cellular RNA, and the pools of ATP, UTP, and uridine 5'-diphospho-N-acetyl glucosamine were significantly increased 13-51% in 48-h diabetics. Nucleotide precursor incorporation was significantly increased only in uracil ribonucleotides. The increase in uracil ribonucleotide pool exceeded the degree of cell hypertrophy. Our studies indicate that renal hypertrophy and specific increases in uracil ribonucleotide synthesis precede functional changes in early diabetes. Renal metabolic changes may be the critical primary factors in diabetic nephropathy.

Animals↗
PubMed1999

First 20 months' experience with use of metformin for type 2 diabetes in a large health maintenance organization.

OBJECTIVE: To assess adherence to prescribing guidelines, continuation rates, population effects on glycemic control, and occurrence of lactic acidosis during the first 20 months of the availability of metformin in a large health maintenance organization. RESEARCH DESIGN AND METHODS: A retrospective cohort study was performed in the 90,000-member diabetes registry of Kaiser Permanente, northern California. Principal study measures were the proportions of patients started on metformin who met prescribing guidelines (previously on sulfonylureas, HbA1c, obesity, creatinine), the change in HbA1c at 6 months after starting metformin, and hospitalization rates for lactic acidosis. RESULTS: A total of 9,875 patients received metformin during this interval. At least 74% were previously treated with sulfonylureas alone, 81% had baseline HbA1c > or = 8.5%, 71% were obese, and 99% had a serum creatinine < or = 1.5 mg/dl. Among patients on sulfonylureas at baseline, those starting metformin had significantly lower HbA1c levels 6 months later than those not started, after adjustment for age, sex, and the higher baseline levels in those started (adjusted difference: 0.5%, P < 0.0001). Patients starting metformin as initial monotherapy also improved significantly, but patients previously treated with insulin (with or without sulfonyl-ureas) had slightly higher follow-up HbA1c levels than similar patients not starting metformin. Continuation of metformin at 12 months was significantly higher for patients previously treated with sulfonylureas than other groups. One probable case of lactic acidosis was identified during 4,502 person-years on metformin. CONCLUSIONS: Adherence to prescribing guidelines was relatively high during metformin's first 20 months of availability. Glycemic control improved substantially for patients previously treated with sulfonylureas. Lactic acidosis was rare.

Adolescent↗
PubMed1976

Why control blood glucose levels?

The controversy as to the relationship between the degree of control of diabetes and the progression of the complications of the disease has not been solved. However, in this review, various studies suggesting a relationship between the metabolic abnormality and the diabetic complications are examined. The disadvantages of the uncontrolled diabetes mellitus can be divided into two major categories-short-term and long-term. The short-term disadvantages of controlled diabetes mellitus include the following: (1) ketoacidosis and hyperosmolar coma; (2) intracellular dehydration; (3) electrolyte imbalance; (4) decreased phagocytosis; (5) immunologic and lymphocyte activity; (6) impairment of wound healing; and (7) abnormality of lipids. The long-term disadvantages of uncontrolled diabetes melitus include the following: (1) nephropathy; (2) neuropathy; (3) retinopathy; (4) cataract formation; (5) effect on perinatal mortality; (6) complications of vascular disease; and (7) the evaluation of various clinical studies suggesting the relationship of elevated blood glucose levels and complications of diabetes mellitus. It is suggested that until the question of control can absolutely be resolved, the recommendation is that the blood glucose levels should be controlled as close to the normal as possible.

Acidosis↗
PubMedDate not supplied

[Role of local factors in the pathogenesis of diabetic retinopathy].

The pathogenesis of diabetic retinopathy includes the following components actual at a local level: diffuse retinal hypoxia leading to increase in the retina of anaerobic energy processes, development of local acidosis causing venous congestion, increased permeability of retinal capillaries and veins, impairment of the structure of vascular walls, development of foci of deep retinal hypoxia and of proliferative changes. These disorders develop in succession and mutually aggravate each other. A noticeable role belongs to deteriorated evacuation of the products of abnormal metabolism which depends on the existence of a solid barrier (pigmented epithelium, Bruch's membrane) between the retina and choroid and on the venous congestion and impaired liquid circulation in the vitreous body. A dichotomic type of division of the central retinal artery and absence of anastomoses between its branches facilitate the appearance of foci of retinal hypoxia. Local pathogenetic therapy of diabetic retinopathy should be aimed at removal of at least one out of three factors: hypoxia, acidosis, or venous congestion. This does not make less important the treatment of general metabolic disorders characteristic of diabetes mellitus.

Acidosis↗
PubMed2000

[Should the occurrence of a first coronary event change the management of diabetes?].

The coronary morbi-mortality is particularly high in type 2 diabetes, which represents the vast majority of all diabetes. Hyperglycemia is an independent vascular risk factor in the short and long-term. The relationship between the degree of hyperglycemia and vascular risk is linear with no threshold effect. The occurrence of a first coronary event is an occasion, though late, to review the management of all risk factors in diabetic patients. In these patients, intensive insulin therapy administered in the acute phase of infarction reduces cardiovascular mortality by 30% at 1 and 3 years. There are no specific studies of secondary prevention by optimal therapy of diabetes, but, in the UKPDS, the treatment of hyperglycemia with sulfonylurea or insulin only marginally reduced the number of cardiovascular events. On the other hand, treatment of obese patients with metformin significantly reduced the incidence of myocardial infarction and of mortality diabetes related. These results, though observed with the same level of glycemic control as in the other treatment groups, suggest a cardio-protective effect of metformin itself. These beneficial effects should be weighed up against the potential risk of lactic acidosis which still limits the widespread use of metformin in with coronary heart disease patients. Follow-up studies show that diabetic with coronary heart disease patients do not receive all effective therapeutic inventions in secondary prevention and that the treatment of hyperglycemia is often neglected. Close collaboration between cardiologists and diabetologists is necessary to improve the management of type 2 diabetes.

Acidosis, Lactic↗
PubMed1999

Lactic acidosis in metformin therapy.

The biguanide drugs metformin and phenformin have been linked in the past to lactic acidosis, a metabolic condition associated with high rates of mortality. Although concern over the hyperlactataemic effect of phenformin led to the withdrawal of this drug from clinical practice in the 1970s, the situation with metformin has been less clear. Retrospective data indicate that, in metformin-treated patients with lactic acidosis, neither the degree of hyperlactataemia nor accumulation of metformin is of prognostic significance. Furthermore, the lowest rates of mortality were seen in patients with high plasma concentrations of metformin, which has led to the hypothesis that the drug may confer some benefit, linked to an increase in vasomotility, in such cases. Overall, it appears that mortality in patients receiving metformin who develop lactic acidosis is linked to underlying disease rather than to metformin accumulation, and that metformin can no longer be considered a toxic drug in this respect. These findings are likely to be of considerable relevance to the management of patients with type 2 (non-insulin-dependent) diabetes mellitus, especially where such patients are elderly.

Acidosis, Lactic↗