OBJECTIVETo observe the effects of Relinqing granules (powder of Polygonum capitatum extract) on the bacterial pyelonephritis model in rats.

METHODThe rat bacterial pyelonephritis model was induced by injecting the escherichia coli ATCC-25922 into kidney parenchyma. The rats were divided ramdamly into Relinqing groups(52.32, 26.16 g x kg(-1)), norflorin group (0.03 g x kg(-1)), model group and normal control group, and were given experimental drugs by gastrogavage. The contents of leucocytes (WBC), occult bloo (BLD), glucose (GLU), protein (PRO), ketones, bilirubin and urobilinagen in urine were determined.

RESULTAs compared with the model group, Relinqing granules 6.0 g x kg(-1) (crude drug 52.32 g x kg(-1)) could decrease significantly the contents of WBC and BLD in urine and, however, had no markedly effects on the other biochemical parameters of urine.

CONCLUSIONRelinqqing granule has significant effects of decreasing urine WBC and BLD on the bacterial pyolonephritis in rats.

Animals ; Anti-Infective Agents, Urinary ; isolation & purification ; pharmacology ; Bilirubin ; urine ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Escherichia coli Infections ; urine ; Female ; Glycosuria ; urine ; Ketones ; urine ; Leukocyte Count ; Male ; Occult Blood ; Plants, Medicinal ; chemistry ; Polygonum ; chemistry ; Proteinuria ; urine ; Pyelonephritis ; urine ; Rats ; Rats, Sprague-Dawley

A 21-year-old man with diabetic ketoacidosis (DKA) displayed short and clubbed fingers and marked eyebrow, which are typical of Hajdu-Cheney Syndrome (HCS). Laboratory findings confirmed type 1 diabetes mellitus (DM). After conservative care with hydration and insulin supply, metabolic impairment was improved. Examinations of bone and metabolism revealed osteoporosis and craniofacial abnormalities. The mutation (c.6443T>G) of the NOTCH2 gene was found. The patient was diagnosed with HCS and DM. There may be a relationship between HCS and DM, with development of pancreatic symptoms related to the NOTCH2 gene mutation.
Adult ; Bone Density ; Craniofacial Abnormalities/complications/radiography ; Diabetes Mellitus, Type 1/*complications/diagnosis ; Diabetic Ketoacidosis/complications/genetics ; Glycosuria ; Hajdu-Cheney Syndrome/*complications/diagnosis/radiography ; Humans ; Ketone Bodies/urine ; Male ; Mutation ; Osteoporosis/complications/radiography ; Receptor, Notch2/*genetics ; Young Adult

OBJECTIVESTo investigate the effects of cadmium exposure on insulin expression in rats.

METHODSEighteen adult SD rats were administered cadmium subcutaneously (0.5, 1.0, and 2.0 mg/kg x bw). The effects on endocrine of pancreas were assessed. The levels of cadmium and zinc in pancreas, blood and urine glucose, serum insulin and urine NAG (N-acyetyl-beta-glucosaminidase) were determined. The gene expressions of metallothionein (MT) and insulin were also measured, and the oral glucose tolerance tests (OGTT) were carried out.

RESULTSThe contents of cadmium in pancreas in cadmium-treated rats were higher than that in the control group, which was associated with slight increase of zinc in pancreas. Cadmium-exposed rats (1.0 and 2.0 mg/kg x bw) demonstrated a marked glucose intolerance. But the levels of serum insulin did not change significantly after cadmium administration, and the UNAG had no change in Cd-treated group. The gene expression of insulin decreased in 1.0 and 2.0 mg/kg x bw cadmium-exposed groups, compared with the control group. The expression of MT-I was higher in the groups exposed to 1.0 and 2.0 mg/kg x bw cadmium while the expression of MT-II was higher in the group exposed to 2.0 mg/kg x bw cadmium.

CONCLUSIONSCadmium may be accumulated in the pancreas, resulting in the change of the expression of insulin, MT-I and MT-II genes. Cadmium can influence the biosynthesis of insulin, but does not induce the release of insulin. The dysfunction of pancreas occurs earlier than that of kidney after administration of cadmium.

Animals ; Base Sequence ; Blood Glucose ; analysis ; Cadmium ; toxicity ; DNA Primers ; Gene Expression ; drug effects ; Glucose Tolerance Test ; Glycosuria ; urine ; Insulin ; blood ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction

Intensive glucose control increases the all-cause mortality in type 2 diabetes mellitus (T2DM); however, the underlying mechanisms remain unclear. We hypothesized that strict diet control to achieve euglycemia in diabetes damages major organs, increasing the mortality risk. To evaluate effects on major organs when euglycemia is obtained by diet control, we generated a model of end-stage T2DM in 13-week-old Sprague-Dawley rats by subtotal pancreatectomy, followed by ad libitum feeding for 5 weeks. We divided these rats into two groups and for the subsequent 6 weeks provided ad libitum feeding to half (AL, n=12) and a calorie-controlled diet to the other half (R, n=12). To avoid hypoglycemia, the degree of calorie restriction in the R group was isocaloric (g per kg body weight per day) compared with a sham-operated control group (C, n=12). During the 6-week diet control period, AL rats ate three times more than rats in the C or R groups, developing hyperglycemia with renal hyperplasia. R group achieved euglycemia but lost overall body weight significantly compared with the C or AL group (49 or 22%, respectively), heart weight (39 or 23%, respectively) and liver weight (50 or 46%, respectively). Autophagy levels in the heart and liver were the highest in the R group (P<0.01), which also had the lowest pAkt/Akt levels among the groups (P<0.05 in the heart; P<0.01 in the liver). In conclusion, glycemic control achieved by diet control can prevent hyperglycemia-induced renal hyperplasia in diabetes but may be deleterious even at isocaloric rate when insulin is deficient because of significant loss of heart and liver mass via increased autophagy.
Albuminuria/urine ; Animals ; *Autophagy ; Cholesterol, HDL/blood ; Diabetes Mellitus, Experimental/blood/*diet therapy/*pathology/urine ; Diet/*adverse effects ; Eating ; Glycosuria/urine ; Insulin/blood ; Liver/*pathology ; Male ; Myocardium/*pathology ; Organ Size ; Proto-Oncogene Proteins c-akt/metabolism ; Rats, Sprague-Dawley ; Serum Albumin/analysis

Adult Fanconi syndrome is characterized by variable abnormalities caused by renal proximal transport defects, resulting in glycosuria, aminoaciduria, bicarbonaturia, uricosuria and phosphaturia. A 57-year-old man with kappa-light chain multiple myeloma, undergoing chemotherapy with prednisolone and melphalan for 17 month, was admitted with spontaneous femoral neck fracture and was consulted due to polyuria and refractory metabolic acidosis immediately after hemiarthroplasty. The laboratory values showed normal anion gap metabolic acidosis with normal urinary anion gap, hypokalemia, hypouricemia, hypophosphatemia at the time of consultation. After partial correction of acidemia, the fractional excretion of HCO3- was 11.9%, it was interpreted as proximal renal tubular acidosis. 24-hour urine collection showed increased level of excretion for most aminoacids. Diffuse osteopenia and multiple compression fractures on spine were detected on radiological examinations. Also, osteoporosis and osteomalacia was suggested during his clinical course. After the diagnosis of Fanconi syndrome was made, treatment was started with sodium bicarbonate, potassium citrate, calcitriol, calcium carbonate along with phosphate rich diet. Laboratory abnormalities were corrected and refractory multiple bone pain was ameliorated with these treatment.
Acid-Base Equilibrium ; Acidosis ; Acidosis, Renal Tubular ; Adult ; Bone Diseases, Metabolic ; Calcitriol ; Calcium Carbonate ; Diet ; Fanconi Syndrome ; Femoral Neck Fractures ; Fractures, Compression ; Glycosuria ; Hemiarthroplasty ; Humans ; Hypokalemia ; Hypophosphatemia ; Hypophosphatemia, Familial ; Melphalan ; Middle Aged ; Multiple Myeloma ; Osteomalacia ; Osteoporosis ; Polyuria ; Potassium Citrate ; Prednisolone ; Sodium Bicarbonate ; Spine ; Urine Specimen Collection