High sucrose diet induces morphological, structural and functional impairments in the renal tubules of Drosophila melanogaster: A model for studying type-2 diabetes mediated renal tubular dysfunction

2020 ◽  
Vol 125 ◽  
pp. 103441
Author(s):  
Lavi Rani ◽  
Sanjay Saini ◽  
Neha Shukla ◽  
Debapratim Kar Chowdhuri ◽  
Naveen Kumar Gautam
2014 ◽  
Vol 123 (01) ◽  
pp. e1-e1 ◽  
Author(s):  
Shuai-yao. Lu ◽  
Su-dong. Qi ◽  
Yuan. Zhao ◽  
Yan-yan. Li ◽  
Feng-mei. Yang ◽  
...  

2014 ◽  
Vol 123 (01) ◽  
pp. 19-26 ◽  
Author(s):  
Shuai-yao. Lu ◽  
Su-dong. Qi ◽  
Yuan. Zhao ◽  
Yan-yan. Li ◽  
Feng-mei. Yang ◽  
...  

2013 ◽  
Vol 60 (3) ◽  
pp. 261-274 ◽  
Author(s):  
Koji Nojima ◽  
Ken Sugimoto ◽  
Hironori Ueda ◽  
Naru Babaya ◽  
Hiroshi Ikegami ◽  
...  

PEDIATRICS ◽  
1957 ◽  
Vol 20 (2) ◽  
pp. 337-357
Author(s):  
Carolyn F. Piel

As indicated in the preceding sections of this review, it seems evident that renal diabetes insipidus, renal glycosuria, "cystinuria" and renal hyperchloremic acidosis are unquestionably renal tubular diseases. Vitamin D resistant rickets has tentatively been placed in the same category although it is recognized that the evidence for this classification is not yet thoroughly convincing. All of the findings of the Fanconi syndrome seem actually to represent a summation of the single tubular diseases, except "cystinosis." Known renal tubular dysfunction fails to explain the cystine-storage disease, cystinosis.


2019 ◽  
Vol 10 (6) ◽  
pp. 3282-3290 ◽  
Author(s):  
Jie Tu ◽  
Guanhui Liu ◽  
Xitao Cao ◽  
Shuyun Zhu ◽  
Qiang Li ◽  
...  

In the present study, the hypoglycemic effects of wheat bran alkyresorcinols were investigated in type 2 diabetes mellitus mice induced by a high-fat/high-sucrose diet combined with low dose streptozotocin.


PEDIATRICS ◽  
1960 ◽  
Vol 26 (1) ◽  
pp. 75-85
Author(s):  
Gunnar B. Stickler ◽  
Alvin B. Hayles ◽  
Marschelle H. Power ◽  
John A. Ulrich

Observations on two girls in whom an unusual type of chronic renal insufficiency developed many months after the onset of nephrotic syndrome are reported. Each patient became free of edema in spite of persistent massive proteinuria. Growth was retarded and rickets and attacks of tetany developed. The chemical disturbances of the blood were characterized by hypocalcemia, hypokalemia, azotemia and metabolic acidosis. Hyposthenuria, proteinuria, amino-aciduria, and minimal erythrocyturia, cylindruria and glycosuria were present. Healing of the rickets and cessation of attacks of tetany followed the administration of vitamin D and calcium salts. Prednisone was administered to one patient and thereafter proteinuria decreased and renal tubular function improved. Both girls are relatively asymptomatic 11 and 9 years after the onset of nephrotic syndrome, although they are rather small and still have evidence of renal disease. It is possible that cells of the renal tubules have been damaged as a result of prolonged massive proteinuria.


2011 ◽  
Vol 14 (2) ◽  
pp. 82-85
Author(s):  
Dilyara Makhmutrievna Khakimova ◽  
Adelya Nailevna Maksudova ◽  
Il'dar Gazimdzhanovich Salikhov

Aim. To study renal functional reserve and partial functions in patents with type 2 diabetes mellitus in the absence of renal lesionsMaterials and methods. We examined 42 patients (17 men and 24 women) aged 38-69 (mean 49.8?8.3) years with DM2 4.6?2.6 yr in duration.Control group comprised 32 practically healthy subjects. Intrarenal hemodynamics was estimated from RFR values. Ethanolamine, uric acid, Ca,and P levels were measured in sera and 24-hr urine; daily excretion of ammonia and aminonitrogen in the urine was determined. Results. The patients were divided into 2 groups based on the results of RFR measurement. FRF remained unaltered in 21 patients (mean 60.7?27.6%)and decreased in the absence of filtration reserve in 20 (-25.8?23.4%). Correlation analysis revealed the relationship of lipid metabolism and abdominalobesity with the renal tubular function and intraglomerular hemodynamics. Conclusion. Examination of DM2 patients without clinical and laboratory signs of renal lesions revealed compromised function of all nephron compartments,viz. intraglomerular hypertension, impaired stability of renal cell membranes, and tubular dysfunction. The latter is related to hemodynamic disturbances.


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