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

The liver and beta cells function in a negative feedback loop, which appears to have a predominant role in regulating both the basal plasma glucose and insulin concentrations. The degree of basal hyperglycemia in diabetes probably provides a bioassay of both the effect of a reduction in insulin secretory capacity and the degree of insulin resistance. A mathematic model of the interaction of insulin deficiency and insulin resistance has been constructed, based on the known response characteristics of the beta cells to glucose, and of plasma glucose and insulin control of hepatic and peripherpal glucose flux. The degree to which beta cell deficiency increases basal plasma glucose reflects the hyperbolic shape of the normal insulin secretory response to different glucose concentrations. The height of basal plasma insulin is a function of the degree of insulin resistance. From the basal plasma insulin and glucose concentrations, the model provides an estimate of the degree to which both beta cell deficiency and insulin resistance contribute to diabetes. The predictions arising from the model are in accord with experimental data in man and in animals. In normal-weight diabetics who do not have increased insulin resistance, the model predicts that more than 85% of beta cell function has to be lost for the basal plasma glucose to rise to 6 mmol/liter, but a further 5%--10% loss increases the basal plasma glucose to over 10 mmol/liter. In a third of a consecutive series of 65 newly presenting, uncomplicated diabetics, both normal weight and obese, the analysis from the model suggested that insulin resistance, rather than beta cell deficit, was the predominant feature.
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PMID:Insulin deficiency and insulin resistance interaction in diabetes: estimation of their relative contribution by feedback analysis from basal plasma insulin and glucose concentrations. 38 29

Injections of rabbit antiserum to rat lymphocytes reversed hyperglycemia in 36 percent of spontaneously diabetic rats (Bio Breeding/Worcester) and prevented diabetes in susceptible nondiabetic controls. These findings strengthen the hypothesis that cell-mediated autoimmunity plays a role in the pathogenesis of diabetes in this animal model that mimics many morpholigic and physiologic characteristics of human insulin-dependent diabetes mellitus.
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PMID:Spontaneous diabetes mellitus: reversal and prevention in the BB/W rat with antiserum to rat lymphocytes. 38 19

Are long-term complications secondary to diabetes or do they appear independently? This question has an important bearing, particularly for the physician and the patient who must achieve optimum control of hyperglycemia. Over the last 10 years, many epidemiological and biochemical studies have shown close links between hyperglycemia and the wide range of factors involved in the development of long-term complications.
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PMID:[Hyperglycemia and diabetic complications]. 39 Jun 94

The aims were to see whether p-hydroxymercuribenzoate (PMB) administration affects the serum insulin concentration in mice in vivo, whether the transitory hyperglycemia induced in fed mice by treatment with PMB is affected by L-leucine, tolbutamide, D-mannoheptulose or insulin, and whether PMB affects the B-cell toxicity of alloxan. A significant decrease in the serum insulin concentration was found 1 and 2 h following PMB injection in fed and starved mice. PMB-induced hyperglycemia was abolished by pre-treatment with L-leucine and tolbutamide, but not by pre-treatment with D-mannoheptulose, or by post-treatment with insulin. Pre-treatment of fed mice with PMB caused potentiation of the initial hyperglycemia following alloxan, but inhibited the second hyperglycemic phase. These findings indicate that PMB treatment of mice has a transient inhibitory influence upon insulin secretion, and protects against the development of alloxan diabetes.
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PMID:p-Hydroxymercuribenzoate-induced hyperglycemia: influence of pre- and post-treatment with L-leucine, tolbutamide, D-mannoheptulose, insulin and alloxan. 39 87

The need for special dietary products marketed for use by individuals with diabetes mellitus and the safety and efficacy of certain nutritive sweetener substitutes for sucrose are reviewed. Special foods for individuals with diabetes mellitus are not necessary to achieve the dietary objectives recommended by leading United States and European authorities. They can be achieved conveniently and at minimum expense through enlightened choices of commonly available food items. At present, specific and unique characteristics of food products with special therapeutic properties for diets of diabetic individuals cannot be delineated or defined on rational nutritional grounds. Such terms as "diet", "dietetic", and "diabetic" on food labels have no uniform meaning for consumers, and diabetologists have observed that patients tend to consume such foods without regard to their energy content. Some consumers regard the reduced-calorie and low-calorie prepared food products as convenient in diets for weight reduction and diabetes although their use in dietary management of diabetes has no therapeutic basis other than weight reduction and maintenance. When fed as pure substances to fasted subjects, the nonglucose carbohydrate nutritive sweeteners, fructose, xylitol, and sorbitol, are absorbed relatively slowly and produce less postprandial hyperglycemia and insulin response than sucrose or glucose. Adequate studies of their long-term effectiveness when ingested as part of mixed meals have not been conducted. Although these sucrose substitutes are generally considered safe, the significance of recent information on possible carcinogenicity of oral xylitol in long-term feeding studies has not been fully evaluated. In view of the lack of certain essential information on the long-term effectiveness of various diets in preventing or mitigating the chronic debilitating complication of diabetes, suggestions for future research are included.
Diabetes Care
PMID:The need for special foods and sugar substitutes by individuals with diabetes mellitus. 40 Jan 33

The glucagon-secreting A cell is a vital component of the organ system which regulates the distribution of fuel--the islets of Langerhans. Bihormonal control of glucoregulation through a push-pull system maintains the glucose concentration of extracellular fluid within narrow limits irrespective of glucose flux rates through relative equality of glucose influx and efflux. This equality requires appropriate secretion mixtures of the biologic antagonists, insulin and glucagon, directed by a glucose sensor. In severe diabetes, there are virtually no B cells and A cells are in contact largely with other A cells and their glucose-sensing capacity is lost. The A cell hypersecretes and in most juvenile type diabetics aggressive therapy with insulin fails to restore it to normal. Glucagon is a factor in the development of endogenous hyperglycemia, and ketoacidosis. Its suppression may provide a possible approach in the future pharmacologic management of diabetic hyperglycemia.
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PMID:Role of glucagon in diabetes. 40 69

In normal man, the fasting state is characterized by release of alanine and glutamine from muscle and in situ muscle catabolism of branched chain amino acids (lecucine, isoleucine, and valine). The alanine released by muscle is utilized by the liver for gluconeogenesis. Muscle nitrogen repletion occurs during protein feeding primarily by means of selective hepatic escape and muscle uptake of branched chain amino acids in ingested protein. In the diabetic, amino acid catabolism is exaggerated in the fasting state as reflected by increased uptake of alanine by the liver for gluconeogenesis and accelerated branched chain amino acid catabolism in muscle. After protein feeding, uptake of branched chain amino acids by muscle is reduced and these amino acids accumulate in increased amounts in arterial blood. Protein feeding also exaggerates the hyperglycemia of diabetes by causing an increase in hepatic glucose production. Diabetes is thus characterized by accelerated protein catabolism during fasting as well as diminished nitrogen repletion and hyperglycemia after protein feeding. The hyperketonemia of diabetes may however, have a restraining influence on protein catabolism thereby reducing alanine availability for gluconeogenesis.
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PMID:Amino acid and protein metabolism in diabetes mellitus. 40 71

We investigated the importance of glucagon in the development of diabetic ketoacidosis by withholding insulin from six patients with juvenile-type diabetes and four totally pancreatectomized subjects. Patients were fasting and had previously been maintained on intravenous insulin for 24 hours. In diabetic patients plasma glucagon concentrations rose sharply after withdrawal of insulin, and the increases were accompanied by a rise in blood ketone concentration of 4.1+/-0.7 (S.E.M.) and blood glucose concentration of 12.5+/-1.8 mmol per liter by 12 hours. In the pancreatectomized patients, despite the absence of measurable glucagon, blood ketones rose by 1.8+/-0.8 and blood glucose by 7.7+/-1.5 mmol per liter. Thus, glucagon is not essential for the development of ketoacidosis in diabetes, as has previously been suggested, but it may accelerate the onset of ketonemia and hyperglycemia in situations of insulin deficiency.
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PMID:Ketoacidosis in pancreatectomized man. 40 53

In 6 diabetic rats about 1,000 isolated islets of Langerhans were transplanted into the liver with little effect on the uninsulinism and hyperglycemia. Subsequently, a second transplantation resulted in a decrease of blood sugar to normal and in a reversal of the loss in body weight. Finally, in animals who had reversed to diabetes again, a third islet transplantation was performed. These rats with a total of 3,100 islets showed a decrease in the glucose levels from 250-305 to 110 +/- 27 (X +/- SEM) mg/100 ml. The insulin level after glucose stimulations was measured at 27 less than X less than 35 micromicron/ml.
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PMID:Multiple transplantation of islets of Langerhans. 41 20

In alloxan-treated diabetic rats, plasma renin activity (PRA) is decreased. One possible mechanism that may explain the decreased PRA is an increased delivery of sodium to the macula densa produced by the glucose osmotic diuresis, resulting in decreased renin release. To evaluate this possible mechanism, rats with phlorhizin diabetes, which produces a glucose osmotic diuresis without hyperglycemia, were studied and compared with rats with alloxan-induced diabetes. Whereas phlorhizin-treated rats had low blood glucose and alloxan-treated rats had elevated glucose, the glucose osmotic diuresis was similar in the two groups. PRA and plasma renin concentration (PRC) were significantly increased in the phlorhizin group. In the alloxan group, PRA was decreased and angiotensin II sensitivity increased, both significantly. Plasma renin substrate (PRS) remained adequate in each group. These results suggest that the decreased PRA in alloxan-induced diabetes is due neither to factors associated with the glucose osmotic diuresis including changes in renal tubular sodium not to decreased PRS.
Diabetes 1979 Feb
PMID:Renin-angiotensin system in phlorhizin compared with alloxan diabetes in the rat. 42 68


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