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Query: UMLS:C0011849 (diabetes)
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Recent information indicates that the capacity of man to store carbohydrate energy by transformation into fatty acids synthetized de novo is very limited in adipose tissue as well as in liver and intestine. This seems to be in contrast to other species such as the rat where de novo fatty acid synthesis can be induced to a high capacity of glucose removal. This leaves man with a limited capacity to store excess carbohydrate. The remaining possibilities are both the main glycogen stores in liver and in muscle. The latter is by far the largest. The capacity of muscle to assimilate glucose is dependent on its glycogen content that in turn is dependent on previous glycogen depletion to supply energy for muscle contraction. Man might, thus, be uniquely limited in the capacity to dispose of extra carbohydrate in the sedentary state. This might speculatively be thought to be an explanation for a carbohydrate excess syndrome in the sedentary state that may well increase the risk for obesity, hyperinsulinemia, and diabetes mellitus. The logical treatment for such a syndrome then is either a decreased intake of energy as carbohydrate or an increased disposal of carbohydrate energy by exercise. Exercise has, indeed, been shown to have such effects both after physical training programs and, perhaps more pertinent to the question, during a few days after a single exercise bout that has consumed a large amount of muscle glycogen.
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PMID:Carbohydrate storage in man: speculations and some quantitative considerations. 72 37

It was taken 32 male Wistar rats, weighting between 130 g and 150 g, free feeding, to study the total and specific activities of lactase, invertase and maltase of small intestine of rats. The animals were divided by chance in 3 experimental and 1 control group. 1. group--Aloxanic diabetes rats: treated with 1 unit of NPH insulin every day: after the 4th day of aloxane administration, all rats were killed. 2. group--Aloxanic diabetes rats--treated for 5 days with 1 unit of NPH insulin every day; after the 5th day until the 7th they were treated with 4 units of NPH insulin and were also killed. 3. group--Hyperinsulinism rats--Normal rats were treated for 4 days with 4 units of NPH insulin every day. After the 5th day they were killed. 4. group--Control group--Normal rats, free feeding. They were observed during 4 days and were also killed. The results showed that none difference was observed in the 4 groups of rats about the total and specific activities of lactase, invertase and maltase of the small intestine. In this study, all the animals with aloxanic diabetes were treated with insulin. Then, it is possible that the insulin inhibited the stimulator effect of the diabetes upon the dissacaridases of the small intestine of the rats.
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PMID:[Insulin and disaccharidases levels of the small intestine of the rat (author's transl)]. 74 51

Diabetes mellitus occurs in many animals species. However, only a few have been utilized in systematic studies designed to answer unsolved problems associated with the disorder in man such as molecular basis, pathogenesis of the vascular and neural lesions, and the roles of diet, exercise and obesity. Among the animal models available, rodents have been studied most thoroughly for a number of reasons: a) short generation time (sexually mature at about 3 mo of age, gestation time 21 days) and life-span is approximately 3 yr; b) hyperglycemia and/or obesity is known to be inherited in several species; c) environmental factors can be controlled easily in the laboratory because of small size; and d) economic considerations. The better-known rodent diabetes/obesity syndromes may be categorized as follows: 1) hyperglycemic with ketoacidosis, nonobese (Chinese hamster, South African hamster); 2) hyperglycemic with insulin hypersecretion, moderate obesity and may develop ketoacidosis (diabetic mouse (db/db), spiny mouse, sand rat); and 3) less pronounced hyperglycemia with hyperinsulinemia, insulin "resistance" and marked obesity (obese (ob/ob), yellow (Ay) and New Zealand obese (NZO) mice, and the Zucker "fatty" rat). The PBB/Ld mouse, described here in detail for the first time, is a new strain of mouse that also fits into the latter category. Members of this strain following maturity develop an obesity that is characterized by increasing cellularity of adipose tissue, increased serum immunoreactive insulin, reduced glucose tolerance, fatty liver, and hyperlipidemia. Therefore, this strain of mouse represents another model for study of adult onset obesity.
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PMID:Animal models of diabetes and obesity, including the PBB/Ld mouse. 77 Jan 97

Sand rats develop a diabetes-like syndrome, connected with temporary hyperinsulinism, when fed a rat laboratory chow diet. The conversion of proinsulin to insulin is not disturbed in these animals. Sand rat islets do not secrete newly synthesized (pro) insulin preferentially. Time course and glucose response of [3H]-leucine incorporation are different between islets of sand rats and Wistar rats.
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PMID:[(Pro)insulin biosynthesis of isolated islands of Langerhans in the sand rat and Wistar rat]. 79 54

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
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PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48

Spontaneous hyperglycemia, hyperinsulinemia and obesity are common features for at least one period of the lifetime in some strains of mice. Both genetic and environmental factors are involved in the pathogenesis of the diabetes-like syndrome, making these strains excellent models for studies in both obesity and diabetes-like states. The metabolic peculiarities can be due to a dominant gene, as for the yellow obese, or a single recessive gene, as in the obese and the diabetes mouse; or they can be of polygenic origin, as for the KK and the NZO mouse. However, the severity of the metabolic disorder is due to the interaction of the mutant genes iwth modifiers in the bat genes themselves. Studies on the pathophysiology and biochemistry of these animals have revealed interstrain differences, different patterns of development of the metabolic disorder, and different degrees of severity of the diabetes-like syndrome. Although the primary causes of the syndrome remain unclear in some strains, an involvement of hypothalamic feeding centers has been implicated.
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PMID:Laboratory animals exhibiting obesity and diabetes syndromes. 83 44

In 158 obese children, aged from three months to 15 years, blood glucose, immunoreactive insulin, and free fatty acid levels were measured during a standard oral glucose tolerance test carried out prior to treatment. The results were analyzed for the total sample as well as for three age groups: 0-5 years, 6-10 years, and 11-15 years and compared with those of 70 normal-weight children matched for age and sex. Glucose tolerance is normal in the obese children. It is different from the controls only two hours after glucose loading, when a slight but significant elevation is found. The glucose levels at one and two hours are significantly higher in the obese children of group III than in the younger ones. Fasting F.F.A. levels are similar in normal and obese children, but the F.F.A. decrease following glucose absorption is significantly diminished in the obese. The F.F.A. levels of the youngest obese are significantly higher than those of the older ones. A constant and important hyperinsulinism, fasting and postabsorptive, is demonstrated in obese children of all ages, even before five years and at the beginning of obesity. Age- and sex-related differences in insulin secretion are much more marked in the obese than in normal children. The degree of hyperinsulinemia is related to the degree of obesity, but not to its duration. The results suggest that hyperinsulinism is associated with obesity from its onset rather than being a long-term consequence of overweight. However, the origin of hyperinsulinism in obesity and the mechanism of insulin resistance still remain obscure.
Diabetes 1977 Feb
PMID:Blood glucose, insulin, and free fatty acid levels during oral glucose tolerance tests in 158 obese children. 83 67

A new automated potentiometric method for the determination of colipase was developed, taking advantage of the reactivation of purified lipase, in the presence of bile salt and at pH 6.5. High-fat and high-starch diets induced an opposite regulation of lipase and amylase in the rat pancreas. At the same time, the level of colipase was not influenced by nutrition. During fasting and in alloxan diabetes, the specific activity of lipase almost doubled, that of amylase decreased sharply, and colipase was not affected in the rat pancreas. In obese-hyperglycemic mice, suffering from obesity, hyperinsulinism, and moderate diabetes, there was also no regulation of pancreatic colipase. Thus, at variance with a number of hydrolases, there was no dietary or hormonal adaptation of colipase. However, this was probably without any bearing on intraluminal lipolysis. Indeed, comparison of lipase and colipase activities in pancreas and in small intestine suggests that colipase concentration is not a limiting factor of intraluminal lipolysis. The molecular mechanism of this assumption is discussed on the basis of in vitro studies.
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PMID:Lack of adaptation of pancreatic colipase in rats and mice. 84 20

Alterations of carbohydrate metabolism were studied in infants of insulin dependent diabetic mothers and in small for date babies with and without prenatal dystrophy. Glucose assimilation (Kt-value) and insulin secretion after i. v. glucose load were examinated on the 1st, 3rd, and 5th day of life. Infants of diabetic mothers showed the highest Kt-values, fasting insulin levels and insulin peaks of all patients examinated. Hyperinsulinism and Kt-values decreased from the 1st to the 3rd day and from the 3rd to the 5th day. In this group the infants of mothers with strictly controlled diabetes showed lower Kt-values, lower insulin peaks and less pronounced cushingoid facies. Small for date babies, on the other hand, had a reduced glucose tolerance on the first day, which normalised up to the 3rd day. The glucose tolerance in small for date babies with prenatal dystrophy, however, showed a tendency to deteriorate again from the 3rd to the 5th day with decreasing Kt-values as well as reduced insulin secretion, which was well documented in two cases. Deterioration of pancreas function and failing adaption to post partum nutrition is put forward as a tentative explanation.
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PMID:[Carbohydrate metabolism of infants with prenatal dystrophy and infants of diabetic mothers. Glucosetolerance and insulinsecretion in the first week of life (author's transl)]. 87 Aug 67

The response of plasma insulin concentration to an oral glucose tolerance test (OGTT) and to the maximum stimulatory effect obtained with administration of glucose, glucagon and tolbutamide was studied in 24 siblings of diabetic children and in ten obese children. Five siblings of patients with diabetes sound to have chemical diabetes had hyperinsulinism during the OGTT. Serum insulin concentrations during the maximum stimulation of the beta cells in the children with chemical diabetes, although diminished at 15 minutes, were considered not significantly different from controls. Obese children had hyperinsulinism during the OGTT and the maximum stimulation of the beta cell. The data suggest that hyperinsulinism may precede or accompany carbohydrate intolerance in siblings of diabetic children.
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PMID:Maximum stimulation of insulin secretion in children with chemical diabetes and obesity. 94 38


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