Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitrogen (N) sparing and even equilibrium have been achieved in obese subjects with all-protein weight-reducing very low energy diets (VLED) apparently independently of the content of essential amino acids. This study assessed whether the metabolic response observed at week 3 of an all-protein VLED with 46% of amino acids (aa) as essential was modified during week 4, when consuming a protein source that provided 16% of amino acids as essential. Six healthy obese subjects (BMI: 35.3 +/- 1.3 kg/m2, weight 90 +/- 9 kg) were given a 1.72 MJ (400 kcal) all protein (93 g) VLED and a multi-vitamin-mineral supplement daily for four weeks. During weeks 1 to 3, the protein was casein-soy (46% essential aa) and during week 4, tryptophan- and methionine-supplemented collagen hydrolysate (16% essential aa). At week 3, decreases in plasma glucose, insulin, cholesterol, blood pH and bicarbonate, and increases in plasma free fatty acids, serum urea, uric acid and blood and urine ketones occurred compared to baseline. These adaptations were unchanged at week 4. N balance returned toward equilibrium by day 23 remaining at values close to 0 despite the change in diet composition. Mean negative N balance did not differ between weeks 3 and 4 (-1.1 +/- 0.5 g vs. -0.6 +/- 0.5 g/day) and neither did mean urinary ammonium N excretion (0.71 +/- 0.08 vs. 0.73 +/- 0.07 g/day). Urinary urea N excretion tended to increase with the collagen-based diet reflecting the greater proportion of N in this protein source (18 vs. 15%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The metabolic response to two very low energy diets (VLED) of differing amino acid composition during weight reduction. 133 70

Histological and immunohistochemical studies were carried out on the pancreas of twelve cattle of insulin-dependent diabetes mellitus (IDDM). They showed clinical signs such as persistent hyperglycemia, glycosuria and decreased glucose tolerance, and some cases accompanied with or without ketonuria. Histopathologically, eight cattle were diagnosed as chronic IDDM, while others were acute IDDM. The most characteristic lesions of the pancreas in chronic IDDM showed a decrease in the size and number of pancreatic islets, interlobular and interacinar fibrosis, mild lymphocytic insulitis, and vacuolation of a few islets. Almost all cells in the atrophied islets had a small amount of ungranulated cytoplasm. Immunohistochemical examination revealed that the atrophied islet cells did not react to anti-insulin antibody, but occasionally reacted to anti-glucagon or somatostatin antibodies. A few solitary islets with mild lymphocytic infiltration, necrotic islets with occasional calcification, and atrophied islets with mild fibrosis were also observed. A few islets consisted of many islet cells with vacuolated cytoplasm including a small number of insulin-positive granules. Accumulation of glycogen granules was occasionally observed in these islets. Islet fibrosis was due to the proliferation of collagen fibers reactive to both anti-collagen type I and type III antibodies. In acute IDDM, the major islets consisted of the cells with vacuolated cytoplasm indicating the degranulation of islet cells. These islets contained many islet cells with shrunken cytoplasm and karyorrhectic nuclei. Lymphocytic infiltration was frequently observed in the islets which consisted of many islet cells having karyorrhectic nuclei and vacuolated and severely degranulated cytoplasm. Immunohistochemically, islet cells with vacuolated cytoplasm had a small amount of insulin-positive granules, suggesting severe degranulation of beta-cells. An increase in acinar islet-cells and proliferation of ductal epithelial cells showing insulin-immunoreactivity were observed. Bovine IgG-immunoreactive islet cells were frequently seen in the vacuolated islets. In summary, pathological observations suggested that beta-cells were being destroyed by an inflammatory process which selectively affected the pancreatic islets. Lymphocytic insulitis and anti-bovine immunoreactive islet cells were thought to be the most significant changes in determining the etiology and pathogenesis of bovine IDDM, and suggested their role in anti-islet autoimmunity in this form of diabetes.
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PMID:Histopathological and immunohistochemical analysis of the endocrine and exocrine pancreas in twelve cattle with insulin-dependent diabetes mellitus (IDDM). 1045 4

We describe a new rat model of autoimmune diabetes that arose in a major histocompatibility complex congenic LEW rat. Spontaneous diabetes in LEW.1WR1 rats (RT1(u/u/a)) occurs with a cumulative frequency of approximately 2% at a median age of 59 days. The disease is characterized by hyperglycemia, glycosuria, ketonuria, and polyuria. Both sexes are affected, and islets of acutely diabetic rats are devoid of beta-cells, whereas alpha- and delta-cell populations are spared. The peripheral lymphoid phenotype is normal, including the fraction of ART2(+) regulatory T-cells. We tested the hypothesis that the expression of diabetes would be increased by immunological perturbation of innate or adaptive immunity. Treatment of young rats with depleting anti-ART2.1 monoclonal antibody increased the frequency of diabetes to 50%. Treatment with the toll-like receptor 3 ligand polyinosinic:polycytidylic acid increased the frequency of diabetes to 100%. All diabetic rats exhibited end-stage islets. The LEW.1WR1 rat is also susceptible to collagen-induced arthritis but is free of spontaneous thyroiditis. The LEW.1WR1 rat provides a new model for studying autoimmune diabetes and arthritis in an animal with a genetic predisposition to both disorders that can be amplified by environmental perturbation.
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PMID:LEW.1WR1 rats develop autoimmune diabetes spontaneously and in response to environmental perturbation. 1612 63