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Query: UMLS:C0011849 (diabetes)
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Male and female virgin rats and breeder rats with naturally-occurring diabetes, hypertension and arteriosclerosis, were made severely diabetic with a single, subcutaneous injection of alloxan (10 mg/100 g b.w.), after an 18 h fast. During five months of unrelenting diabetes, some animals became obese while others became emaciated. Only the emaciated animals survived but they were blind, their adrenal glands were hemorrhagic, hypertrophied and thrombosed, thymi involuted, kidneys swollen, hearts reduced in size while testes and ovaries were atrophic. Serum CPK, SGOT and SGPT were elevated concomitant with extensive cardiovascular damage, hepatic steatosis and generalized catabolism. Circulating triglycerides and free fatty acids were markedly elevated with total cholesterol only slightly increased. BUN and serum calcium levels were also greatly elevated. Sub-normal Cmpd. B levels indicated impaired adrenal steroidogenesis. Virgin rats developed arteriosclerosis and male and female breeder rats showed exacerbation of their pre-existing aortic sclerosis as well as P.A.N. lesions in their small-sized arteries. It is believed that severe diabetes causes exacerbation of the endogenous hormonal milieu resulting from abnormal hypothalamic-pituitary-adrenal function induced by repeated breeding, which conditions the connective tissue components of the arterial wall of rats toward accelerated degenerative changes.
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PMID:Polyarteritis nodosa induced in arteriosclerotic, male and female breeder rats by chronic alloxan diabetes. 1 32

From a group of 424 patients with histologically verified fatty liver 92 patients without diabetes mellitus and alcohol abuse were subjected to follow-up examination for 3 1/2 years. 56 patients underwent second liver biopsy at this time; 20 of these patients had shown marked fatty liver at the initial liver biopsy examination. These 20 patients with marked fatty liver and 25 further patients with moderarte fatty liver could be followed up 5 and 7 1/2 years later; the clinical examination, the various liver function tests, liver scan and blind liver biopsy did not show any evidence of progression of fatty liver towards chronic inflammatory liver disorders or precirrhotic states. This clinical study therefore suggests the harmlessness of non-alcoholic fatty liver.
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PMID:Follow-up study on patients with non-alcoholic and non-diabetic fatty liver. 49 27

Liver function and liver biopsy findings were studied in a selected group of 29 overweight patients. Fatty liver, fatty hepatitis, fatty fibrosis and fatty cirrhosis were seen with equal frequency. Diabetes was also present with an equal incidence in each of these four pathologic groups. Lipoprotein abnormalities, particularly type IV hyperlipoproteinemia, were found mostly in the two groups with the lesions with less fibrosis (fatty liver and fatty hepatitis). The pathologic picture resembled that of alcohol and postjejunoileal bypass-induced liver diseases suggesting a common denominator in these three conditions.
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PMID:Fatty liver hepatitis and cirrhosis in obese patients. 50 94

A relationship between the occurrence of fatty liver and moderate alcohol intake, maturity onset diabetes, overweight--and combinations of these three factors--was searched for in 112 patients. Fifty-three of 59 patients with moderate alcohol consumption, 49 of 57 overweight patients, and 42 of 51 diabetic patients had fatty liver. Patients who had a moderate alcohol consumption or suffered from a combination of diabetes and overweight were found to have a significantly higher frequency and degree of fatty liver than patients in the control group. Diabetes alone, and overweight alone were not significantly related to fatty liver. Whether the diabetic state was overt of latent, there was no influence on the frequency or degree of fatty liver. A correlation between the degree of overweight and the degree of fatty liver was found only in the group of overweight patients with moderate alcohol consumption. The degree of fatty liver produced by the combination of overweight and diabetes was not significantly increased by moderate alcohol consumption.
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PMID:Fatty liver in patients with moderate alcohol consumption, diabetes mellitus and overweight. 59 49

Liver function tests were performed in severe and mild diabetic rats and under the influence of ATP. In mild diabetics the serum cholesterol was significantly increased, while in severe diabetes the serum cholesterol was significantly lower than in mild diabetes. The decreased serum cholesterol in severe diabetes may be an indication for the development of fatty liver. The serum alkaline phosphatase and serum bilirubin were significantly increased in both the severe and mild diabetic states, while the thymol turbidity test was insignificantly changed in both states of diabetes. Serum albumin was significantly decreased in 10 days mild diabetes, while it was insignificantly changed in 48 hrs severe diabetic animals. The effect of ATP was investigated in mild diabetes. ATP resulted in a significant increase in serum albumin and a decrease in total globulins with the resultant increase in A/G ratio. The serum alkaline phosphatase exhibited a significant reduction under the influence of ATP. The elevated cholesterol of mild diabetic rats remained significantly elevated and was not reduced by ATP, though the fat content of the liver showed a significant reduction. This may be due to more rapid mobilisation of fat from the liver under the influence of ATP. ATP showed no significant effect on serum bilirubin and thymol turbidity test. the histopathological examination of the liver revealed that administration of ATP to alloxan diabetic rats had a beneficial effect. It resulted in disappearrance of the fat globules from the liver cells.
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PMID:Effect of ATP on liver function tests in experimental diabetes. 65 50

Plasma lipids and lipoproteins, glucose tolerance, plasma insulin response to glucose load, and liver function were examined in 81 relatives of 12 index cases with primary endogenous hypertriglyceridemia, hyperinsulinemia, and hepatic steatosis, as well as in 90 nonrelatives, including the spouses, as controls. Insulin hypersecretion (with or without glucose intolerance), endogenous hypertriglyceridemia, and abnormal liver function suggesting hepatic steatosis were shown to exist in the relatives mostly in combined fashion. Correlation analysis and stepwise multiple regression analysis revealed that the combined disorder developed on the basis of obesity. The incidence of diabetes mellitus was significantly high in the relatives (14.8 per cent) as compared with the normal Japanese population (3.5 per cent). Although the vertical transmission of the combined disorder was noted in almost all pedigrees, the frequency distribution analysis of insulin response, glucose tolerance, and plasma triglyceride showed the histograms of these variables similarly skewed to the right as compared with those of the controls, with no apparent bimodality. In view of the hitherto suggested role of insulin in triglyceride metabolism, it is concluded that hyperinsulinemia coupled with obesity seems to be the basic trait of this form of familial hypertriglyceridemia and hepatic steatosis, though the mode of transmission remains to be elucidated.
Diabetes 1978 Jun
PMID:Interactions of obesity and glucose-stimulated insulin secretion in familial hypertriglyceridemia. 65 14

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

Oral glucose tolerance tests (100 g glucose) and the intravenous tolbutamide test were carried out. The glucose tolerance was seen to be disordered even in acute infectious hepatitis, but returning to normal when cured. If chronic hepatitis develops, however, the proportion of manifest diabetes increases to 7.2% in chronic persistent hepatitis and to 16.3% in chronic progressive hepatitis, while 30% each have latent diabetes. The glucose tolerance is most impaired in fatty liver (stage III) and in active cirrhosis of the liver with portal hypertension, where more than half of all patients present manifest or latent diabetes. Conversely, glucose tolerance improves even in chronic hepatitis and in cirrhosis of the liver as the inflammatory activity subsides. The main cause for the development of "liver diabetes" is therefore likely to be the activity of the inflammatory process, the extent of portal hypertension, disorders of glucose regulation in the liver and the increased insulin inactivation in the cirrhotic liver.
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PMID:[Disorders of glucose tolerance in 2600 histologically confirmed acute and chronic liver patients (author's transl)]. 81 Jun 95

In 15 mongrel dogs, a mixture of exocrine and endocrine pancreatic tissue obtained by a simple procedure was implanted into the liver of the same animal through a branch of the portal vein. Five animals with partial pancreatectomy were used for a morphological study. In a second group of ten dogs, 5 delayed and 5 immediate pancreatectomies were performed. No diabetes appeared after the pancreatectomy. The subsequent blood glucose and insulin levels remained within or close to the normal range for several weeks in 9 animals and up to 10 months in a last one, still alive. In 9 out of 10 animals, the long term study was limited between 6 and 17 weeks by the development of a malnutrition syndrome with hepatic steatosis due to the lack of exocrine secretory function because of the pancreatectomy. The last animal still alive developed the malnutrition syndrome after a second complementary resection of a small pancreatic fragment left along the duodenum. This last animal without diabetes at the 45th week suggests that the endocrine function of the autotransplanted pancreatic tissue could be maintained over a long period of time.
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PMID:[Prevention of diabetes in pancreatectomised dogs by autotransplantation of pancreatic tissue in the liver]. 81 64

In order to investigate the combined effects of diabetes and hypertension on the pathogenesis of cardiovascular disease, adult male and female SHR rats which develop hypertension spontaneously were given a single, 10 mg or 15 mg/100 g body wt. injection of alloxan s.c. to induce moderate or severe diabetes. Insulin was deliberately withheld. Animals were examined by autopsy daily for 7 days post-alloxan and after 4 and 8 weeks. Mortality was high--only 52% of the males survived as against 80% of the females. Most deaths occurred on Day 5 and were associated with adrenal haemorrhage and hyperplasia, thymus galnd involution, fatty liver and marked hypotension despite elevated aldosterone levels. During the first week, corticosterone levels increased significantly in the male; in females they showed little change. After 4 weeks, the severly diabetic animals became emaciated and moribund; corticosterone and aldosterone levels fell to very low levels despite adrenal hyperplasia. The beta cells of the moderately diabetic animals eventually lost their ability to secrete insulin and these animals too became cachetic and moribund with concomitant elevation of lipid, glucose and BUN levels, as well as myocardial infarction, fatty liver, and generalized hyalin arteriolo-, arterio-, and nephrosclerosis. It is suggested that the combined hormonal and metabolic alterations of diabetes and hypertension reinforced one another in these spontaneously hypertensive rats, leading to intense stimulation of the hypothalamic-pituitary-adrenal system, the exacerbation of those cardiovascular degenerative changes known to be associated with uncontrolled diabetes or hypertension, eventual impaired adrenocortical steroidogenesis, hypotension and death.
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PMID:Alloxan diabetes in spontaneously hypertensive rats: gravimetric, metabolic and histopathological alterations. 86 Nov 67


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