Insulärer und Insulinresistenter Diabetes

Falta, W.; Boller, R

doi:10.1007/bf01736348

Cited by 46 publications

(19 citation statements)

References 12 publications

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“…Much of the attention around metabolic flexibility is because of its implication in insulin resistance, a concept first advanced by Wilhelm Falta and published in Vienna in 1931 as a possible underlying cause of type 2 diabetes (Falta and Boller, 1931). During the ensuing 85 years insulin resistance has evolved to become generally accepted as the predominant factor leading to type 2 diabetes, and the most probable single link among a constellation of cardiometabolic risk factors known as the metabolic syndrome linking obesity, type 2 diabetes and cardiovascular disease (Reaven, 1988).…”

Section: Fasting To Feeding - Insulin Resistance As Part Of the Metabmentioning

confidence: 99%

Metabolic Flexibility in Health and Disease

2017

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Summary Metabolic flexibility is the ability to respond or adapt to conditional changes in metabolic demand. This broad concept has been propagated to explain insulin resistance and mechanisms governing fuel selection between glucose and fatty acids, highlighting the metabolic inflexibility of obesity and type 2 diabetes. In parallel, contemporary exercise physiology research has helped to identify potential mechanisms underlying altered fuel metabolism in obesity and diabetes. Advances in ‘omics’ technologies have further stimulated additional basic and clinical-translational research to further interrogate mechanisms for improved metabolic flexibility in skeletal muscle and adipose tissue with the goal to prevent and treat metabolic disease.

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Section: Fasting To Feeding - Insulin Resistance As Part Of the Metabmentioning

confidence: 99%

Metabolic Flexibility in Health and Disease

2017

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“…In some instances the operation of such factors, for example, liver disease (11,12), thyrotoxicosis (13), and pituitary disease (14) can be clearly demonstrated. In others, in whom there is simply a resistance to test doses of insulin, extra-pancreatic factors have been assumed (4,9,10). In the present state of our knowledge such assumptions do not appear to be justified.…”

Section: Resultsmentioning

confidence: 93%

The Response of Diabetics to a Standard Test Dose of Insulin

Klatskin¹

1938

J. Clin. Invest.

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That some diabetics improve on high carbohydrate diets is an established fact (1, 2). The selection of suitable patients for this type of diet has, until the present, been one of trial and error. Recently MacBryde (3) has made an attempt to select cases on the basis of insulin sensitivity. He studied the response of a small group of diabetics to a standard test dose of insulin and concluded that they fell into two groups, the relatively insulin-resistant and the relatively insulinsensitive. The resistant group gained tolerance on high carbohydrate diets while the sensitive group did not. In addition, the patients showing insulin-resistance were usually older, frequently obese, often had vascular hypertension and showed little tendency to acidosis. The relatively sensitive group were usually younger, often thin, had as a rule low blood pressure and were more prone to develop acidosis and coma. Although the insulin requirement of the resistant group was larger, the sensitive group were looked upon as more serious, judged by their tendency to acidosis. On the basis of a somewhat different test, Himsworth (4) classified diabetics in a similar manner, but concluded from his experimental findings and clinical data that insulin-sensitive patients tolerated high carbohydrate diets better than did the insulin-insensitive.Since these two investigators appear to have come to diametrically opposite conclusions in regard to the relationship between insulin sensitivity and response to high carbohydrate diets, it was felt worth while to study this problem further. The purpose of the present investigation has been to study a relatively large group of diabetics with respect to their blood sugar response to a standard test of insulin, and to correlate, if possible, insulin sensitivity with their clinical characteristics and responses to diets of variable carbohydrate content. METHOD OF STUDYFifty of a total of 197 patients attending the adult Diabetic Clinic of the Strong Memorial Hospital were chosen for this study. Each had previously had a complete physical examination, blood count, urinalysis, and Wassermann reaction. They represented a fair crosssection of the total clinic population and were arbitrarily selected from amongst those who had attended the clinic for at least five months and who had been most cooperative and regular in their attendance. None was suffering from infection at the time of the studies. Cases in which the diagnosis of diabetes mellitus was at all questionable were subjected to a sugar tolerance test and were accepted only if they had typical diabetic responses (Cases 7, 25, 40, 45).Each patient was subjected to an "insulin tolerance test" and classified as relatively insulin-sensitive or relatively insulin-resistant. His past record in our clinic and on any admission to the hospital was then studied and analyzed. These studies constitute the basis for this report. The patients had previously been followed from 5 to 123 months, an average of 42 months each, and had usually been seen at monthly interval...

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“…The first test used to distinguish between the two main forms of diabetes was response to insulin. Wilhelm Falta and other investigators in Vienna drew attention to the existence of insulin-sensitive and -resistant forms of diabetes (7). Insulinsensitive patients readily suppressed urinary excretion of glucose and developed hypoglycemia in response to a few units of insulin, whereas withdrawal of insulin rapidly resulted in glycosuria and ketosis.…”

Section: The Heterogeneity Of Diabetesmentioning

confidence: 99%

The Discovery of Type 1 Diabetes

Gale

2001

Diabetes

126

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The etiological heterogeneity of idiopathic diabetes has been recognized for 25 years, and subdivision into type 1 and type 2 diabetes is fundamental to the way we think about the disease. Review of the literature suggests that the concept of type 1 diabetes as an immunemediated disease emerged rapidly over the period from 1974 to 1976 and showed many of the features of a classic paradigm shift. A few key observations triggered recognition and acceptance of the new paradigm, but the necessary context was provided by scientific developments in areas mainly unrelated to diabetes. The disease paradigm established by 1976 is still widely accepted, and its essential features have been modified only in detail by the revolution in molecular biology that has occurred over the intervening period. Notwithstanding, some of the underlying assumptions remain imprecise, unchallenged, or unconfirmed. Appreciation of the historical origin and subsequent evolution of these fundamental concepts could stimulate critical analysis and help prepare the way for a new paradigm. Diabetes 217-226, 2001

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Insulärer und Insulinresistenter Diabetes

Cited by 46 publications

References 12 publications

Metabolic Flexibility in Health and Disease

Metabolic Flexibility in Health and Disease

The Response of Diabetics to a Standard Test Dose of Insulin

The Discovery of Type 1 Diabetes

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