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

Baroreflex function was studied in three groups of adult rabbits. Seven animals were given alloxan (100-200 mg/kg) and became diabetic (group D) with mean blood sugar values of 348 +/- 30 mg/dl. Eight animals were given alloxan, but did not develop significant hyperglycemia (135 mg/dl) (group A). Nine controls (group C) were also studied (glucose, 101 mg/dl). All animals were anesthetized with pentobarbital (30 mg/kg). Blood pressure (BP) and heart rate (HR) responses to bilateral carotid occlusion (BCO) were measured before and after depressor nerve sectioning (DNx) and sinus nerve sectioning (SNx). Before sectioning, BCO caused a rise in BP of 30 +/- 4 mmHg in group C. 35 +/- 3 in group A, and 36 +/- 4 in group D. HR increased about 13 beats/min in each group. After DNx, resting BP increased in group C from 97 to 104 mmHg (P less than 0.005), but no change occurred in the other groups. Responses to BCO were significantly but similarly enhanced in all groups after DNx. HR did not increase in group D. Resting BP increased after SNx only in the controls (group C). Differences in BP elevation with BCO before and after SNx ("pure" reflex response) were identical, averaging about 35 mmHg. Thus, no alteration of BP or HR responses to BCO was identified in early alloxan diabetes. However, resting tone in the buffer nerves may have been less.
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PMID:Carotid sinus reflex function in the alloxan diabetic rabbit. 42 76

The role of metabolic abnormalities in the development of diabetic neuropathy is controversial. To investigate the influence of hyperglycemia on nerve conduction, we studied 20 untreated maturity-onset diabetic patients and 23 normal control subjects of similar age. Nerve conduction velocity of motor (median, peroneal, and tibial) and sensory (median and sural) nerves in diabetic patients was significantly slowed and H-reflex latency time prolonged. Levels of fasting plasma glucose in diabetic subjects were correlated with slowed motor conduction velocity of the median, peroneal, and tibial nerves but not with sensory nerve conduction velocities. Levels of glycosylated hemoglobin, an index of long-term glycemia, were correlated with slowing of peroneal motor conduction velocity in diabetic patients. These associations could not be explained by patient age or duration of diabetes. These findings suggest that the degree of hyperglycemia of untreated maturity-onset diabetes contributes to the motor nerve conduction abnormalities in this disease.
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PMID:Nerve conduction abnormalities in untreated maturity-onset diabetes: relation to levels of fasting plasma glucose and glycosylated hemoglobin. 42 98

We have carried out studies on cultured human fibroblasts in an attempt to trace the origins of age-dependent disorders to the cellular and molecular levels. Three interrelated areas are discussed. First, skin donors with diabetes mellitus (a disease complex that features inappropriate hyperglycemia) produce cultured fibroblasts with a moderate reduction in growth capacity, while two inherited disorders of inappropriate hyperglycemia and premature aging, progeria and Werner syndrome, yield fibroblast cultures with more severely impaired growth capacity. Second, there is a decreased response of progeria level and donor age; evidence is presented that this defective hormone responsiveness in aging cells may reside at the hormone receptor on the surface membrane, the cyclic AMP system, the intracellular enzymatic machinery, or all of these sites. Third, tissue factor, a procoagulant that activates the extrinsic clotting mechanism, is more abundant in cells from the premature aging syndromes of progeria and Werner syndrome. Fibroblast aging in vitro may help to explain various concomitants of normal aging and diabetes mellitus including cell dropout, impairment of hormone responsiveness, and increased atherothrombosis.
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PMID:In vitro studies of age-associated diseases. 42 66

The idea that the gene(s) that cause diabetes mellitus can be expressed in extrapancreatic cells has been examined by tissue culture techniques. Skin biopsies were obtained from 25 normal subjects (N), 26 overt diabetics (D), 16 of juvenile onset (JOD) and 9 of maturity onset (MOD), and 21 subjects genetically predisposed to diabetes (P) on the basis of maturity-onset diabetes in both parents. Each biopsy was subdivided, multiple skin fragments were explanted in vitro, and several parameters of cellular outgrowth were monitored in primary and secondary cultures until cell division ceased because of senescence. In general, the rank order of growth vigor was N greater than P greater than D although differences were often marginal and statistically significant between N and JOD and(or) MOD. Outgrowth of epithelial cells was more vigorous in N explants in early stages, but later, JOD and MOD cells grew better than those of N. Outgrowth of fibroblast cells from N explants was more vigorous both at early and later stages and required less time to achieve maximum percent outgrowth. In secondary cultures, N cells grew faster than the other three groups so that fewer days elapsed between subcultures but significant differences were only seen between N and one or two of the other groups over some of the first seven subcultures. The onset of cellular senescence occurred earlier in P and JOD cultures both in mean population doublings and calendar time. N cultures had a higher percent surviving clones after picking than MOD, and a shorter recloning time than clones of JOD. The replicative life-spans of cultures (mean population doublings +/- SE) were N = 52.54 +/- 2.24, P = 47.84 +/- 2.43, JOD = 47.12 +/- 2.99, and MOD = 46.40 +/- 4.04, but differences did not reach significance for N vs the other three groups. The data demonstrate that cellular growth is impaired in both JOD and MOD types of cultures and to a generally lesser extent in P cultures. This is consistent with intrinsic genetic defects but the possibility that persistent deleterious effects of in vivo pathophysiology contribute alone or in combination cannot be ruled out. Therefore, the diabetic defect(s) can be expressed in extrapancreatic cells of mesenchymal origin. This system should prove useful in exploring the interplay between genetic and environmental factors in diabetes, the mechanisms(s) of hyperglycemia and other metabolic derangements, and the propensity that affected individuals have to develop degenerative diseases.
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PMID:Diabetes mellitus and genetic prediabetes. Decreased replicative capacity of cultured skin fibroblasts. 42 58

A retrospective study of 94 patients, who had had doubtful results in the oral provoked-hyperglycemia test, was made after an average period of 23 months. It was found that 26 patients were diabetic, 34 were normal and 34 were still doubtful. The factors which influence the evolution of these cases are the sex, a family history of diabetes (before 60 years of age), and the return to normal weight of obese patients.
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PMID:[The provoked-hyperglycemia test. Follow-up after two years of 94 cases with doubtful results (author's transl)]. 43 32

The intravenous injection of zinc or manganese chloride immediately before and 15 minutes after alloxan or dithizone prevented the usual hyperglycemia observed 24 hours after induction of diabetes. Injection of zinc chloride in alloxan diabetes led to normalization of sodium while zinc, copper, iron and magnesium remained high and calcium and potassium remained low as in alloxan. In case of dithizone diabetes, the administration of zinc salt led to an increase in serum zinc, magnesium and potassium and to a decrease in serum calcium while the sodium level returned to normal. Manganese plus alloxan led to a normalization of serum zinc, copper, potassium and sodium. In the case of dithizone plus manganese only magnesium was raised while the other elements were unchanged when compared to animals injected with dithizone only. Chromium and cobalt lowered the blood glucose to a certain extent however it did not affect most of the elements. The same changes occurred in all elements as with alloxan or dithizone alone. Pretreatment with ATP led to a normalization of serum zinc, copper, magnesium, sodium and potassium, while in case of iron it remained high and calcium remained low as that found in alloxan diabetic rats.
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PMID:Serum mineral changes due to exogenous ATP and certain trace elements in experimental diabetes. 44 5

Insulin-independent diabetes is a disease characterized by insulin resistance and the patient's concomitant inability to compensate by exaggerated insulin secretion. A primary abnormality in the plasma membrane of the afflicted cells may cause both of these phenomena. Recent studies investigating the mechanism of action of sulfonylurea drugs show that these agents probably exert their antidiabetic action by increasing insulin sensitivity and ameliorating the insulin resistance, rather than by increasing insulin secretion. Dietary treatment alone, though effective in lowering the FPG level, does not ameliorate the insulin resistance of insulin-independent diabetes mellitus. Thus, sulfonylurea drugs appear to be rational therapeutic agents for the treatment of this form of diabetes. Clinical studies confirm the beneficial effects of these drugs in controlling the hyperglycemia of insulin-independent diabetes. Major unresolved questions are (1) Why do primary and secondary failures occur? (2) Is the underlying membrane abnormality progressive? (3) How long are sulfonylureas effective? (4) What is the mechanism of the membrane disturbance and how do sulfonylureas ameliorate it? (5) Do sulfonylureas drugs cause cardiovascular toxicity? The answers to these questions will provide further insight into our understanding of insulin-independent diabetes and will lead to the development of better drugs for its treatment. In the meantime, sulfonylureas are rational agents for the therapy for this disorder, if they are used appropriately.
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PMID:Sulfonylurea drugs and insulin-independent diabetes mellitus. 44 91

Hemoglobin A1c (HbA1c) is a minor component of human hemoglobin resulting from a non enzymatic linkage of glucose with the NH2-terminal amino acid of the beta chain of hemoglobin. Under normal conditions, HbA1c represent about 5% of total hemoglobin. The HbA1c blood concentration increases in direct proportion of the duration and degree of hyperglycemia. Available procedures for measuring HbA1c include column chromatography, high pressure liquid chromatography, a colorimetric procedure based on the formation of 5-hydroxymethylfurfural and isoelectrofocusing. In a group of 138 patients, we have confirmed that HbA1c provides a useful means of evaluating the degree of diabetic control: the highest values have been recorded in cases of poor control, the lowest in cases of excellent control. In the latter case, the HbA1c values recorded were not statistically different from those obtained in a control group of 92 non-diabetic subjects. The interest of evaluating this parameter in diabetes is briefly analyzed.
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PMID:[Hemoglobin A1c and diabetes control (author's transl)]. 44 35

In an attempt to prevent the onset of diabetes, young, genetically prediabetic (but not yet hyperglycemic) Chinese hamsters were treated continuously with insulin via minipump for 4 wk beginning 1 wk before the predicted age of onset of glucosuria (age 7 wk). Continuous insulin infusion which increased the plasma insulin levels by 70%, did not cause hypoglycemia, nor did it reduce the incidence or severity of diabetic symptoms over the ensuing year of observation. In fact, early treatment with exogenous insulin tended to cause increased hyperglycemia and glucosuria. No plasma anti-insulin antibodies were detected 3 and 9 months after stopping insulin treatment.
Diabetes 1979 Jun
PMID:Effect of continuous low-dose insulin treatment on subsequent incidence of diabetes in genetically prediabetic Chinese hamsters. 44 13

Muscle capillary basement membrane width (MCBMW) was measured in 18 myotonic dystrophy patients and compared with that in age- and sex-matched normal and diabetic subjects. The MCBMW in myotonic dystrophy patients (773 +/- 258 A) was significantly thinner than in normal subjects (925 +/- 181 A, P less than 0.05) or in diabetics (1224 +/- 614 A, P less than 0.01). An increase in MCBMW with advancing age was present in all groups but was greatest in the myotonic dystrophy groups (r = +0.59, P less than 0.01). There was no relation between MCBMW and either the degree of glucose intolerance or insulin hypersecretion in the myotonic dystrophy group, though none had fasting hyperglycemia. This is the first report of a condition associated with thinner-than-normal capillary basement membrane.
Diabetes 1979 Jul
PMID:Thin muscle capillary basement membranes in myotonic dystrophy. 44 22


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