glycogen and Kidney-Diseases

Parenteral nutrition has been one of the major advances in clinical medicine in the 20th century. By maintaining or re-establishing optimal nutritional status, one can help to ensure an optimal response to appropriate medical or surgical management of the primary disease process. In order to plan an appropriate nutritional regimen, the health-care provider must be equipped to pursue the following thought processes: Understand the consequences of malnutrition. Identify the patient who may benefit from nutritional support. Assess the underlying clinical and metabolic setting. Assess the current nutritional status. Formulate a goal of nutritional intervention--a therapeutic plan. Determine the route and method of administration; the quantity and source of energy and nitrogen; and requirements for fluid, electrolytes, minerals, vitamins, and trace elements. Monitor the patient. Evaluate the efficacy and determine the duration of therapy.

Topics: Catheterization; Dietary Carbohydrates; Dietary Proteins; Energy Metabolism; Female; Glycogen; Heart Failure; Hepatic Encephalopathy; Humans; Intraoperative Period; Kidney Diseases; Male; Metabolic Diseases; Parenteral Nutrition, Total; Pregnancy; Starvation; Stress, Physiological; Triglycerides

The cerebrohepatorenal syndrome of Zellweger (CHRS) is remarkable not only for a distinctive combination of congenital anomalies, but also for an unusual variety of profound metabolic disturbances. After a discussion of the clinical diagnosis of CHRS, abnormalities in the metabolism of peroxisomes, mitochondria, iron, pipecolic acid, glycogen, bile acids, and organic acids are discussed and related to the clinical and other biochemical findings in the syndrome. Attention is also drawn to syndromes with biochemical or clinical abnormalities similar to those of CHRS. Although the biochemical findings indicate major abnormalities in oxidative metabolism, the primary defect remains obscure.

Topics: Abnormalities, Multiple; Amino Acids, Dicarboxylic; Bile Acids and Salts; Brain Diseases; Glutarates; Glycogen; Humans; Iron; Kidney Diseases; Liver Diseases; Microbodies; Mitochondria; Pipecolic Acids; Syndrome

Renal biopsies have been examined in patients either currently (50 patients) or previously (5 patients) on maintenance lithium therapy for severe affective disorders. In patients currently taking lithium, a distinctive lesion of the distal convoluted tubules and collecting ducts was identified. This lesion consisted of vacuolation and swelling of the cytoplasm with accumulations of PAS positive material; this material was confirmed to be particulate glycogen by light and ultrastructural techniques. This 'lithium-associated' lesion was not present in patients who had discontinued lithium therapy. Prospective studies showed that the accumulation of glycogen occurs in distal tubules and collecting ducts within days of commencing lithium treatment. The relationship of this distinctive lesion to the patchy focal cortical interstitial fibrosis seen in these biopsies remains to be elucidated.

Topics: Adult; Affective Disorders, Psychotic; Aged; Female; Glycogen; Humans; Kidney Diseases; Kidney Tubules; Kidney Tubules, Distal; Lithium; Male; Middle Aged

Topics: Cardiomyopathies; Glucosephosphate Dehydrogenase Deficiency; Glucosidases; Glucosyltransferases; Glycogen; Glycogen Storage Disease; Hepatomegaly; Humans; Kidney Diseases; Liver Cirrhosis; Liver Diseases; Liver Glycogen; Muscular Diseases; Pectins; Polysaccharides; Splenomegaly

Topics: Glycogen; Humans; Kidney Diseases; Myocardium; Shock, Septic; Streptococcal Infections

Diethylene glycol (DEG) exposure poses risks to human health because of widespread industrial use and accidental exposures from contaminated products. To enhance the understanding of the mechanistic role of metabolites in DEG toxicity, this study used a dose response paradigm to determine a rat model that would best mimic DEG exposure in humans. Wistar and Fischer-344 (F-344) rats were treated by oral gavage with 0, 2, 5, or 10g/kg DEG and blood, kidney and liver tissues were collected at 48h. Both rat strains treated with 10g/kg DEG had equivalent degrees of metabolic acidosis, renal toxicity (increased BUN and creatinine and cortical necrosis) and liver toxicity (increased serum enzyme levels, centrilobular necrosis and severe glycogen depletion). There was no liver or kidney toxicity at the lower DEG doses (2 and 5g/kg) regardless of strain, demonstrating a steep threshold dose response. Kidney diglycolic acid (DGA), the presumed nephrotoxic metabolite of DEG, was markedly elevated in both rat strains administered 10g/kg DEG, but no DGA was present at 2 or 5g/kg, asserting its necessary role in DEG-induced toxicity. These results indicate that mechanistically in order to produce toxicity, metabolism to and significant target organ accumulation of DGA are required and that both strains would be useful for DEG risk assessments.

Topics: Acidosis; Alanine Transaminase; Animals; Aspartate Aminotransferases; Blood Urea Nitrogen; Chemical and Drug Induced Liver Injury; Creatine; Dose-Response Relationship, Drug; Ethylene Glycols; Glycogen; Glycolates; Kidney; Kidney Diseases; Liver; Male; Rats, Inbred F344; Rats, Wistar

The redox sensitive glycogen synthase kinase (GSK) 3 has been recently implicated in the pathogenesis of proteinuric glomerulopathy. However, prior studies are less conclusive because they relied solely on chemical inhibitors of GSK3, which provide poor discrimination between the isoforms of GSK3 apart from potential off target activities. In murine kidneys, the β rather than the α isoform of GSK3 was predominantly expressed in glomeruli and distributed intensely in podocytes. By employing the doxycycline-activated Cre-loxP site specific gene targeting system, GSK3β was successfully knocked out (KO) selectively in podocytes in adult mice, resulting in a phenotype no different from control littermates. Electron microscopy of glomeruli in KO mice demonstrated more glycogen accumulation in podocytes but otherwise normal ultrastructures. Upon oxidative glomerular injury induced by protein overload, KO mice excreted significantly less albuminuria and had much attenuated podocytopathy and glomerular damage. The anti-proteinuric and glomerular protective effect was concomitant with diminished accumulation of reactive oxygen species in glomeruli in KO mice, which was likely secondary to a reinforced Nrf2 antioxidant response in podocytes. Collectively, our data suggest that GSK3β is dispensable for glomerular function and histology under normal circumstances but may serve as a therapeutic target for protecting from oxidative glomerular injuries.

Topics: Albuminuria; Animals; Antioxidants; Cells, Cultured; Glycogen; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Immunoblotting; Kidney Diseases; Kidney Glomerulus; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Microscopy, Confocal; Microscopy, Electron, Transmission; Oxidation-Reduction; Podocytes; Reactive Oxygen Species

This study aimed at assessing the effects of Kefir, a probiotic fermented milk, on oxidative stress in diabetic animals. The induction of diabetes was achieved in adult male Wistar rats using streptozotocin (STZ). The animals were distributed into four groups as follows: control (CTL); control Kefir (CTLK); diabetic (DM) and diabetic Kefir (DMK). Starting on the 5th day of diabetes, Kefir was administered by daily gavage at a dose of 1.8 mL/day for 8 weeks. Before and after Kefir treatment, the rats were placed in individual metabolic cages to obtain blood and urine samples to evaluate urea, creatinine, proteinuria, nitric oxide (NO), thiobarbituric acid reactive substances (TBARS) and C-reactive protein (CRP). After sacrificing the animals, the renal cortex was removed for histology, oxidative stress and NOS evaluation. When compared to CTL rats, DM rats showed increased levels of glycemia, plasmatic urea, proteinuria, renal NO, superoxide anion, TBARS, and plasmatic CRP; also demonstrated a reduction in urinary urea, creatinine, and NO. However, DMK rats showed a significant improvement in most of these parameters. Despite the lack of differences observed in the expression of endothelial NO synthase (eNOS), the expression of inducible NO synthase (iNOS) was significantly lower in the DMK group when compared to DM rats, as assessed by Western blot analysis. Moreover, the DMK group presented a significant reduction of glycogen accumulation within the renal tubules when compared to the DM group. These results indicate that Kefir treatment may contribute to better control of glycemia and oxidative stress, which is associated with the amelioration of renal function, suggesting its use as a non-pharmacological adjuvant to delay the progression of diabetic complications.

Topics: Animals; Cultured Milk Products; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Disease Progression; Glucose Tolerance Test; Glycogen; Hyperglycemia; Kidney Diseases; Kidney Tubules; Male; Nitric Oxide; Oxidative Stress; Probiotics; Rats; Rats, Wistar; Streptozocin

Ursolic acid (UA) is a pentacyclic triterpenoid compound that naturally occurs in fruits, leaves and flowers of medicinal herbs. This study investigated the dose-response efficacy of UA (0.01 and 0.05%) on glucose metabolism, the polyol pathway and dyslipidemia in streptozotocin/nicotinamide-induced diabetic mice. Supplement with both UA doses reduced fasting blood glucose and plasma triglyceride levels in non-obese type 2 diabetic mice. High-dose UA significantly lowered plasma free fatty acid, total cholesterol and VLDL-cholesterol levels compared with the diabetic control mice, while LDL-cholesterol levels were reduced with both doses. UA supplement effectively decreased hepatic glucose-6-phosphatase activity and increased glucokinase activity, the glucokinase/glucose-6-phosphatase ratio, GLUT2 mRNA levels and glycogen content compared with the diabetic control mice. UA supplement attenuated hyperglycemia-induced renal hypertrophy and histological changes. Renal aldose reductase activity was higher, whereas sorbitol dehydrogenase activity was lower in the diabetic control group than in the non-diabetic group. However, UA supplement reversed the biochemical changes in polyol pathway to normal values. These results demonstrated that low-dose UA had preventive potency for diabetic renal complications, which could be mediated by changes in hepatic glucose metabolism and the renal polyol pathway. High-dose UA was more effective anti-dyslipidemia therapy in non-obese type 2 diabetic mice.

Topics: Animals; Antineoplastic Agents, Phytogenic; Blotting, Western; Diabetes Complications; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Dyslipidemias; Glucokinase; Glucose; Glucose Transporter Type 2; Glucose-6-Phosphatase; Glycogen; Hyperglycemia; Kidney Diseases; Male; Mice; Mice, Inbred ICR; Mice, Inbred NOD; Polymers; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Signal Transduction; Triterpenes; Ursolic Acid

Cadmium, a well-known environmental pollutant and a toxic transitional metal causes severe damage to many organs, such as liver, kidney, lungs, heart, etc. The current study has been designed to assess the impact of p-coumaric acid, a common dietary polyphenol on cadmium chloride-induced renal toxicity in rats. Therefore, the activities of membrane bound ATPases, mitochondrial TCA cycle and electron transport chain enzymes, gluconeogenic and glycolytic enzymes, and glycogen content were estimated in kidney tissue homogenates of control and experimental rats. In addition, the serum levels of glucose and pro-inflammatory cytokines, such as TNF-α and IL-1β were also estimated. The cadmium chloride administered rats (3 mg per kg per b. wt per s.c.) showed significant decrease in the levels of membrane bound ATPases, mitochondrial TCA cycle and electron transport chain enzymes, glycolytic enzymes, and glycogen content as compared with controls. Conversely, the levels of glucose, gluconeogenic enzymes and pro-inflammatory cytokines (TNF-α, and IL-1β) were found to be increased. However, the administration of p-coumaric acid (100 mg per kg per b. wt per s.c.) along with the cadmium chloride significantly modulated these biochemical and immunological changes to near normal, as compared to cadmium chloride treated rats. Thus, the results provide strong evidence that p-coumaric acid has a protective action against cadmium-induced renal toxicity in rats.

Topics: Adenosine Triphosphatases; Animals; Blood Glucose; Cadmium Chloride; Coumaric Acids; Female; Glycogen; Interleukin-1beta; Kidney; Kidney Diseases; Male; Mitochondria; Oxidative Stress; Polyphenols; Propionates; Rats; Rats, Wistar; Tumor Necrosis Factor-alpha

Diabetic nephropathy is strongly associated with both increased oxidative stress and kidney tissue hypoxia. The increased oxidative stress causes increased kidney oxygen consumption resulting in kidney tissue hypoxia. To date, it has been difficult to determine the role of kidney hypoxia, per se, for the development of nephropathy. We tested the hypothesis that kidney hypoxia, without confounding factors such as hyperglycemia or elevated oxidative stress, results in nephropathy. To induce kidney hypoxia, dinitrophenol (30 mg per day per kg bodyweight by gavage), a mitochondrial uncoupler that increases oxygen consumption and causes kidney hypoxia, was administered for 30 consecutive days to rats. Thereafter, glomerular filtration rate, renal blood flow, kidney oxygen consumption, kidney oxygen tension, kidney concentrations of glucose and glycogen, markers of oxidative stress, urinary protein excretion, and histological findings were determined and compared with vehicle-treated controls. Dinitrophenol did not affect arterial blood pressure, renal blood flow, glomerular filtration rate, blood glucose, or markers of oxidative stress but increased kidney oxygen consumption, and reduced cortical and medullary concentrations of glucose and glycogen, and resulted in intrarenal tissue hypoxia. Furthermore, dinitrophenol treatment increased urinary protein excretion, kidney vimentin expression, and infiltration of inflammatory cells. In conclusion, increased mitochondrial oxygen consumption results in kidney hypoxia and subsequent nephropathy. Importantly, these results demonstrate that kidney tissue hypoxia, per se, without confounding hyperglycemia or oxidative stress, may be sufficient to initiate the development of nephropathy and therefore demonstrate a new interventional target for treating kidney disease.

Topics: Animals; Dinitrophenols; Glucose; Glycogen; Hyperglycemia; Hypoxia; Kidney; Kidney Diseases; Male; Mitochondria; Oxidative Stress; Oxygen Consumption; Rats; Rats, Sprague-Dawley; Renal Circulation; Uncoupling Agents; Vimentin

Diabetes mellitus is a major endocrine disorder and a growing health problem in most countries which can be ameliorated by numerous bio-molecules such as 1alpha,25 dihydroxyvitamin D3 [1alpha,25(OH)2VD3]. With this in mind, the current study investigated the therapeutic and preventive effects of 1alpha,25(OH)2VD3 on diabetes and its side effects: toxicity in liver, pancreas and kidneys. Our results show that administration of 1alpha,25(OH)2VD3 in diabetic rats increased the plasmatic insulin level, favored the normal blood glucose levels and normalized the hepatic glycogen concentration. In addition, 1alpha,25(OH)2VD3 enhanced superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) (by 207, 52 and 72%, respectively) compared to diabetic rats. It also reduced lipid peroxidation and the indices of toxicity in liver and kidneys by significantly decreasing alkaline phosphatases (PAL), aspartate and lactate transaminase (AST and ALT) activities, total and direct bilirubin, triglycerides (TG), cholesterol, creatinine, urea and iron levels in diabetic rats. Moreover, the plasmatic non-enzymatic antioxidant level of HDL-cholesterol, magnesium (Mg), calcium (Ca) and copper (Cu) increased after 1alpha,25(OH)2VD3 administration. The administration of 1alpha,25(OH)2VD3 in diabetic rats protects against alloxan-induced histological changes in pancreas.. from these data, it is concluded that 1alpha,25(OH)2VD3 might be useful for the therapy and prevention of diabetes and the numerous side effects especially toxicity in liver, pancreas and kidneys and this protective effect is more obvious in our preventive experiment.

Topics: Animals; Blood Glucose; Calcitriol; Catalase; Diabetes Mellitus, Experimental; Glutathione Peroxidase; Glycogen; Insulin; Kidney; Kidney Diseases; Lipid Peroxidation; Liver; Liver Diseases; Male; Organ Size; Oxidative Stress; Pancreas; Pancreatic Diseases; Rats; Rats, Wistar; Superoxide Dismutase

The present study has been conducted to evaluate the curative effect of propolis extract, a honey bee-hive product, against acetaminophen (APAP) induced oxidative stress and dysfunction in liver and kidney. Animals were challenged with APAP (2 g/kg, p.o.) followed by treatment of propolis extract (100 and 200 mg/kg, p.o.) once only after 24 h. Release of transaminases, alkaline phosphatase, lactate dehydrogenase, and serum bilirubin were increased, whereas hemoglobin and blood sugar were decreased after APAP administration. Antioxidant status in both the liver and kidney tissues were estimated by determining the glutathione, malondialdehyde content and activities of the CYP enzymes, which showed significant alterations after APAP intoxication. In addition, activities of adenosine triphosphatase, acid phosphatase, alkaline phosphatase, and major cell contents (total protein, glycogen and cholesterol) were also altered due to APAP poisoning. Propolis extract successfully reversed the alterations of these biochemical variables at higher dose. Improvements in hepatorenal histoarchitecture were also consistent with biochemical observations. The results indicated that ethanolic extract of propolis has ability to reverse APAP-induced hepatorenal biochemical and histopathological alterations probably by increasing the antioxidative defense activities due to various phenolic compounds present in it.

Topics: Acetaminophen; Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Antioxidants; Bilirubin; Blood Glucose; Chemical and Drug Induced Liver Injury; Cholesterol; Cytochrome P-450 Enzyme System; Dose-Response Relationship, Drug; Female; Glutathione; Glycogen; Hemoglobins; Kidney; Kidney Diseases; L-Lactate Dehydrogenase; Liver; Liver Diseases; Malondialdehyde; Oxidative Stress; Propolis; Rats; Rats, Sprague-Dawley; Silymarin; Transaminases

This work investigated the preventive effects of ZnCl(2) on renal and hepatic alterations induced by HgCl(2) in young rats. Wistar rats of 3 days old were treated (s.c.) on consecutive days with saline or ZnCl(2) 27 mg/kg/day from the 3rd to the 7th and with saline or HgCl(2) 5.0mg/kg/day from the 8th to the 12th day of life. Pups were sacrificed 24h after the last dose and samples were collected. The creatinine and urea dosages, used as renal parameters, presented increases of 35% and 500%, respectively. The alanine aminotransferase and lactic dehydrogenase activities, used as hepatic parameters, presented a decrease (40%) and no alteration, respectively, by mercury exposure. The glycemia was diminished and the hepatic glycogen was not modified by mercury. All the mercury effects were prevented by zinc. These results suggest that mercury intoxication of young rats alters the renal function but does not modify the hepatic parameters, and previous exposure to zinc is able to avoid the renal damage.

Topics: Alanine Transaminase; Animals; Animals, Newborn; Blood Glucose; Chlorides; Creatine; Female; Glycogen; Kidney; Kidney Diseases; L-Lactate Dehydrogenase; Liver; Male; Mercuric Chloride; Protective Agents; Rats; Rats, Wistar; Urea; Zinc Compounds

In order to investigate the glomerular size and renal localization of apolipoprotein in type Ia glycogen storage disease, a renal biopsy was performed in two proteinuric patients. Histopathological examination of the biopsy specimens revealed focal sclerotic glomerular sclerosis in both patients. The mean glomerular area was 21.6 +/- 11.6 x 10(3) microns 2, indicating enlargement of the glomeruli. Immunohistochemical staining of the specimens for apolipoprotein showed localization of apolipoprotein AI on the inner side of the glomerular capillary wall, and in proximal tubular epithelial cells. In one patient with a history of several episodes of hypoglycemia, treatment with corn starch improved the carbohydrate and lipid metabolic profile and reduced the daily urinary protein excretion from 2.23 to 0.5 g. These results suggest that focal sclerotic glomerular lesions associated with type Ia glycogen storage disease may be related to disorders of carbohydrate and lipid metabolism.

Topics: Adult; Apolipoproteins; Biopsy; Complement C3d; Fats; Glomerular Mesangium; Glycogen; Glycogen Storage Disease Type I; Humans; Immunoglobulin A; Immunoglobulin M; Immunohistochemistry; Kidney; Kidney Diseases; Kidney Glomerulus; Male; Middle Aged

Hypertension and proteinuria were observed in a 2-year-old child with type IA (von Gierke's) glycogen storage disease (GSD). She had evidence of hyperfiltration and had elevated selective renal vein renins. On renal biopsy, increased mesangial cell matrix and cellularity were observed with focal thickening and irregularity of the basement membrane. This case may be representative of the early renal findings in type IA GSD.

Topics: Female; Glycogen; Glycogen Storage Disease Type I; Histocytochemistry; Humans; Hypertension, Renal; Infant; Kidney; Kidney Diseases; Proteinuria

The serologically active moiety of an antigen detected occasionally in pathologic sera by double-diffusion gel precipitation tests, referred to in earlier studies as ubiquitous tissue antigen, was identified as a dextran composed predominantly, if not exclusively, of a(1 leads to 6)-linked glycopyranoses. By means of an enzyme immunoassay, dextran or dextran-like material, which inhibited the binding of antidextran serum to dextran, was detected in sera of several patients with various gastrointestinal (GI) diseases, especially GI ulcers (7/10), and also often in sera of aged people (9/21). However, 2 of 50 normal blood donor sera and a few sera from almost every disease group studied contained low quantities of dextran-like material. The levels of antidextran antibodies of the IgG class were also often elevated among patients with GI diseases and aged people as demonstrated by enzyme immunoassay with dextran T-500 as the solid phase antigen. OD values exceeding the mean plus 2.5 SD of 106 normal blood donor sera were recorded in ;69% of patients with gastric and duodenal ulcers, 40% with ulcerative colitis, 29% with Crohn's disease, 20% with colorectal carcinomas, and in 21% with rheumatoid arthritis. None of 23 children, but 9 of 23 aged people (35%) had elevated antibody levels. It is suggested that absorption of dextrans from food or their production by intestinal bacteria may be facilitated in various GI diseases.

Topics: Adult; Aged; Animals; Antibody Formation; Cattle; Chemical Precipitation; Child; Colonic Neoplasms; Dextrans; Diverticulitis; Epitopes; Glycogen; Humans; Immunodiffusion; Immunoenzyme Techniques; Kidney Diseases; Ostreidae; Rabbits

We found marked accumulation of glycogen in the brain in one case of the cerebro-hepato-renal syndrome (CHRS). Glycogen in the form of beta-particles was deposited freely within the nucleus, perikaryon and cell processes of neurons and glial cells. The changes involved the gray matter diffusely but were more prominent in the cerebral cortex. The patient died at the age of 4 months after a clinical course characterized by severe hypotonia, seizures, and apneic episodes. Other neuropathologic findings were developmental malformations of the central nervous systen (CNS) (pachygyria, polymicrogyria, and hypoplasia of the inferior olives), white matter abnormalities (deficiency in myelination and diffuse accumulation of sudanophilic droplets within glial cells), clusters of peculiar "globoid" histiocytes with pleomorphic lipid inclusions, and microglial nodules in gray and white matter. This unusual combination of findings is regarded as characteristic of the CHRS.

Topics: Brain; Brain Diseases; Cerebral Cortex; Glycogen; Histocytochemistry; Humans; Infant; Kidney Diseases; Liver Diseases; Male; Neuroglia; Neurons; Syndrome

In diabetes mellitus abnormal quantiites of glycoprotein may be formed in the basement membrane of the glomerulus and both renal function and size may increase. It is suggested that these changes, of quite different potential significance, have a common origin an increased rate of uridine-triphosphate synthesis resulting from hyperglycemia.

Topics: Animals; Basement Membrane; Diabetes Complications; Diabetes Mellitus; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Glycogen; Glycoproteins; Humans; Hyperglycemia; Hypertrophy; Kidney; Kidney Diseases; Kidney Glomerulus; Rats; RNA; Sclerosis; Uracil Nucleotides

As a contribution to the aetiology of insufficiency of placenta carbohydrate-histo-chemical investigations of the kyema were per-formed from the 10 th to 14 th week of pregnancy. The studies were carried out on pregnancy products of women with affection of kidneys, circulatory failures, and under cytostatic therapy. For comparison purposes, cases were used where the pregnancy was without organic diseases of the pregnant women. The investigations performed did not prove evidence of an essential alteration of the regulation of carbohydrates in the kyema by maternal disorders or cytostatic treatment during early gravidity.

Topics: Adrenal Glands; Adult; Antineoplastic Agents; Carbohydrates; Cardiovascular Diseases; Decidua; Embryo, Mammalian; Extraembryonic Membranes; Female; Glycogen; Histocytochemistry; Humans; Kidney; Kidney Diseases; Liver; Placenta Diseases; Placental Insufficiency; Pregnancy; Pregnancy Trimester, First; Trophoblasts

Topics: Acyltransferases; Adolescent; Adult; Alkaline Phosphatase; Anemia, Hemolytic; Biliary Tract Diseases; Child; Child, Preschool; Cystic Fibrosis; Erythroblastosis, Fetal; Female; gamma-Glutamyltransferase; Glutamate Dehydrogenase; Glycogen; Hematologic Diseases; Hepatitis A; Humans; Hyperthyroidism; Hypothyroidism; Infant; Infant, Newborn; Kidney Diseases; Leucyl Aminopeptidase; Neoplasms; Oxidoreductases; Pregnancy

Topics: Body Fluids; Cells; Citric Acid Cycle; Diet; Extracellular Space; Glycogen; Hormones; Humans; Hypernatremia; Kidney; Kidney Diseases; Metabolism; Osmolar Concentration; Parenteral Nutrition; Proteins; Sweat Glands; Triglycerides; Water-Electrolyte Balance

Topics: Acid Phosphatase; Adrenal Glands; Animals; Chromaffin System; Cytoplasm; Depression, Chemical; Dogs; Fats; Femoral Artery; Glycogen; Glycosaminoglycans; Heart; Heparin; Histocytochemistry; Injections, Intra-Arterial; Intestine, Small; Kidney; Kidney Diseases; Leukocytes; Liver; Liver Glycogen; Lung; Mononuclear Phagocyte System; Muscles; Necrosis; Penicillins; Peritoneum; RNA; Spleen; Stimulation, Chemical; Stomach; Succinate Dehydrogenase

Topics: Glycogen; Humans; Kidney Diseases; Methods

Topics: Autopsy; Biopsy; Cardiomyopathies; Glucosidases; Glycogen; Glycogen Storage Disease; Glycoside Hydrolases; Humans; Infant; Kidney; Kidney Diseases; Liver; Liver Diseases; Microscopy, Electron; Muscles; Muscular Diseases; Myocardium; Ultracentrifugation

Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Diabetic Nephropathies; Glomerulonephritis; Glycogen; Histocytochemistry; Humans; In Vitro Techniques; Kidney; Kidney Diseases; Microscopy, Electron; Middle Aged; Nephrosis

Topics: Glycogen; Humans; Hypertension; Kidney Diseases

Topics: Glycogen; Humans; Kidney; Kidney Diseases; Kidney Glomerulus; Renal Circulation; Water

Two hundred and seven albino rats were injected subcutaneously with alloxan in doses varying from 140 to 200 mg. per cent per kilo of body weight. Fifty-nine animals which developed hyperglycemia (blood sugar levels above 150 mg. per cent) were observed for periods from 5 days to 32 weeks. Postmortem examination of the kidneys of these diabetic animals revealed glycogen deposition in the loops of Henle and convoluted tubules in 26 rats or 44 per cent. Glycogen could not be demonstrated in the glomeruli. Within the time limits of this experiment (32 weeks) no intercapillary glomerulosclerosis was observed. The following facts were revealed regarding glycogen nephrosis in alloxan diabetes: (a) Its appearance in the kidneys of the diabetic rats depended solely upon the terminal blood sugar levels of these animals. A value of 350 mg. per cent was the critical level, above which glycogen nephrosis was almost invariably demonstrable. With terminal levels below 300 mg. per cent no glycogen nephrosis was found. (b) No relationship existed between the postmortem finding of glycogen nephrosis and the initial blood sugar level, or the maximum height of the hyperglycemia attained by individual rats. (c) The results suggest that glycogen nephrosis is a reversible lesion.

Topics: Alloxan; Animals; Body Weight; Diabetes Mellitus; Diabetes Mellitus, Experimental; Glycogen; Hyperglycemia; Kidney; Kidney Diseases; Kidney Tubules; Nephrosis