glycogen and Proteinuria

The metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending on whether glycogen stores are adequate, inhibits protein synthesis, and results in fatty liver and in elevations in serum triglyceride levels. Increases in high-density lipoprotein cholesterol after ethanol ingestion may explain the lower risk of myocardial infarction and death from coronary disease after moderate drinking. Increases in serum lactate, resulting from the increased NADH/NAD+ ratio, and hyperuricemia, most likely the result of increased turnover of adenine nucleotides, are common transient effects of ethanol ingestion. Causes of vitamin deficiencies in alcoholism are decreased dietary intake, decreased intestinal absorption, and alterations in vitamin metabolism. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde increases the degradation of pyridoxal 5'-phosphate by displacing it from its binding protein and making it susceptible to hydrolysis by membrane-bound alkaline phosphatase. Ethanol decreases hepatic vitamin A concentration and its conversion to active retinal, and modifies renal metabolism of vitamin D.

Topics: Amino Acids; Animals; Ethanol; Fatty Liver, Alcoholic; Folic Acid; Glycogen; Humans; Lactates; Lactic Acid; Lipids; Liver; Proteinuria; Pyridoxine; Rats; Thiamine; Uric Acid; Vitamin A; Vitamin D

Cilnidipine (Cil) is an L/N-type calcium channel blocker (CCB) that is known to provide renal protection by decreasing the activity of the sympathetic nervous system and the renin-angiotensin system (RAS). However, very few studies have evaluated the renoprotective effects of Cil in hypertension complicated by diabetes mellitus. In this study, we compared the effects of cilnidipine and the L-type CCB, amlodipine (Aml), in combination with an angiotensin II receptor blocker (ARB) on diabetic nephropathy that developed as a result of inducing diabetes in hypertensive rats.. Diabetes was induced in 9-week-old male spontaneously hypertensive rats by intraperitoneally injecting them with streptozotocin (40 mg/kg twice) and the rats (8 per group) were randomly assigned to receive valsartan (Val), Cil + Val, Aml + Val, or vehicle for 8 weeks through a gastric tube.. There were no significant differences in systolic blood pressure or plasma parameters between the two combination therapy groups. Blood pressure lowering by neither combination therapy significantly affected the glycemic variables. However, the increased glycogen levels in the kidney as a result of hyperglycemia were significantly suppressed in the groups that received combination therapy, and the increased proteinurea and glomerulosclerosis due to progression of the diabetic nephropathy were significantly suppressed in the Cil + Val group. In addition, a significant decrease in ED-1-positive cells was observed in the Cil + Val group alone.. The results of this study suggested that the L/N-type CCB, cilnidipine, had additive antihypertensive and proteinuria-lowering effects when administered in combination with an ARB, even in type-1 diabetic rats, and that the L-type CCB, amlodipine, did not. Furthermore, combination therapy with cilnidipine and valsartan significantly reduced glycogen accumulation and ED-1-positive cell infiltration, suggesting that cilnidipine suppressed the excessive increase in the activity of the sympathetic nervous system and RAS through N-type calcium channel blockade.

Topics: Amlodipine; Angiotensin II Type 1 Receptor Blockers; Animals; Antihypertensive Agents; Biomarkers; Blood Glucose; Blood Pressure; Calcium Channel Blockers; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Dihydropyridines; Disease Progression; Drug Therapy, Combination; Glomerulonephritis; Glucagon; Glucose Transporter Type 1; Glycated Hemoglobin; Glycogen; Hypertension; Kidney; Male; Norepinephrine; Proteinuria; Rats; Rats, Inbred SHR; Renin-Angiotensin System; Tetrazoles; Transforming Growth Factor beta1; Valine; Valsartan

The aim of the present study is to investigate the antidiabetic properties of oligosaccharides of Ophiopogonis japonicus (OOJ) in experimental type 2 diabetic rats. OOJ was administered orally in doses of 225 and 450 mg/kg body weight to high-fat diet and low-dose streptozotocin (STZ)-induced type 2 diabetic rats for 3 weeks. The results showed that OOJ treatment could increase body weight, decrease organ related weights of liver and kidney, reduce fasting blood glucose level, and improve oral glucose tolerance in diabetic rats. Moreover, increased glycogen content in liver and skeletal muscle, reduced urinary protein excretion, higher hepatic GCK enzyme activity, lower hepatic PEPCK enzyme activity, enhanced GLP-1 level, decreased glucagon level and alleviated histopathological changes of pancreas occurred in OOJ-treated diabetic rats by comparison with untreated diabetic rats. This study demonstrates, for the first time to our knowledge, that OOJ exerts remarkable antidiabetic effect in experimental type 2 diabetes mellitus, thus justifying its traditional usage.

Topics: Animals; Blood Glucose; Body Weight; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Diet, High-Fat; Fasting; Glucagon; Glucagon-Like Peptide 1; Glucose Tolerance Test; Glycogen; Hypoglycemic Agents; Liver; Male; Muscle, Skeletal; Oligosaccharides; Ophiopogon; Organ Size; Proteinuria; Rats; Rats, Sprague-Dawley

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

Topics: Animals; Diabetes Mellitus, Experimental; Glycogen; Islets of Langerhans Transplantation; Kidney; Kidney Function Tests; Kidney Glomerulus; Male; Proteinuria; Rats; Transplantation, Isogeneic; Water-Electrolyte Balance

Topics: Acetyl Coenzyme A; Acetyl-CoA Carboxylase; Adipose Tissue; Amino Sugars; Animals; ATP Citrate (pro-S)-Lyase; Carbon Radioisotopes; Cholesterol; Deoxyadenosines; Epididymis; Fatty Acid Synthases; Fatty Acids; Fatty Acids, Nonesterified; Glycogen; Ligases; Liver; Malate Dehydrogenase; Male; Nephrotic Syndrome; Oxo-Acid-Lyases; Proteinuria; Rats; Time Factors; Triglycerides

Topics: Bacteriuria; Blood Glucose; Diabetic Nephropathies; Glomerular Filtration Rate; Glycogen; Glycosuria, Renal; Growth Hormone; Humans; Hypertension, Renal; Insulin; Kidney; Kidney Tubules; Proteinuria; Urinary Bladder, Neurogenic; Urinary Tract Infections; Urination Disorders

Topics: Adult; Complement System Proteins; Creatinine; Fluorescent Antibody Technique; Glucose Tolerance Test; Glycogen; Glycosuria; Humans; Immunoglobulin G; Kidney Glomerulus; Kidney Tubules; Male; Microscopy, Electron; Nephrotic Syndrome; Proteinuria

Topics: Animals; Blood Glucose; Brain; DNA; Female; Fetus; Gestational Age; Glycogen; Hypertension, Renal; Lipid Metabolism; Liver; Lung; Placenta; Pregnancy; Pregnancy Complications, Cardiovascular; Proteins; Proteinuria; Rats