Structure and segmental localization of glycogen in the diabetic rat kidney

Diabetes ◽  
1993 ◽  
Vol 42 (6) ◽  
pp. 891-900 ◽  
Author(s):  
P. Holck ◽  
R. Rasch
Keyword(s):  
Rat Kidney ◽  
Diabetic Rat

scholarly journals Potassium channel contributions to afferent arteriolar tone in normal and diabetic rat kidney

2008 ◽  
Vol 295 (1) ◽  
pp. F171-F178 ◽  
Author(s):  
Carmen M. Troncoso Brindeiro ◽  
Rachel W. Fallet ◽  
Pascale H. Lane ◽  
Pamela K. Carmines
Keyword(s):  
Potassium Channel ◽  
Rat Kidney ◽  
The Other ◽  
Diabetic Rat ◽  
Channel Blockers ◽  
Juxtamedullary Nephron ◽  
Afferent Arterioles ◽  
Arteriolar Tone ◽  
Constrictor Response

We previously reported an enhanced tonic dilator impact of ATP-sensitive K+ channels in afferent arterioles of rats with streptozotocin (STZ)-induced diabetes. The present study explored the hypothesis that other types of K+ channel also contribute to afferent arteriolar dilation in STZ rats. The in vitro blood-perfused juxtamedullary nephron technique was utilized to quantify afferent arteriolar lumen diameter responses to K+ channel blockers: 0.1–3.0 mM 4-aminopyridine (4-AP; KV channels), 10–100 μM barium (KIR channels), 1–100 nM tertiapin-Q (TPQ; Kir1.1 and Kir3.x subfamilies of KIR channels), 100 nM apamin (SKCa channels), and 1 mM tetraethylammonium (TEA; BKCa channels). In kidneys from normal rats, 4-AP, TEA, and Ba2+ reduced afferent diameter by 23 ± 3, 8 ± 4, and 18 ± 2%, respectively, at the highest concentrations employed. Neither TPQ nor apamin significantly altered afferent diameter. In arterioles from STZ rats, a constrictor response to TPQ (22 ± 4% decrease in diameter) emerged, and the response to Ba2+ was exaggerated (28 ± 5% decrease in diameter). Responses to the other K+ channel blockers were similar to those observed in normal rats. Moreover, exposure to either TPQ or Ba2+ reversed the afferent arteriolar dilation characteristic of STZ rats. Acute surgical papillectomy did not alter the response to TPQ in arterioles from normal or STZ rats. We conclude that 1) KV, KIR, and BKCa channels tonically influence normal afferent arteriolar tone, 2) KIR channels (including Kir1.1 and/or Kir3.x) contribute to the afferent arteriolar dilation during diabetes, and 3) the dilator impact of Kir1.1/Kir3.x channels during diabetes is independent of solute delivery to the macula densa.

scholarly journals Candesartan augments compensatory changes in medullary transport proteins in the diabetic rat kidney

2008 ◽  
Vol 294 (6) ◽  
pp. F1448-F1452 ◽  
Author(s):  
Mitsi A. Blount ◽  
Jeff M. Sands ◽  
Kimilia J. Kent ◽  
Tekla D. Smith ◽  
S. Russ Price ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Renin Angiotensin System ◽  
Transport Proteins ◽  
Diabetic Rat ◽  
Angiotensin Ii Receptor ◽  
Volume Depletion ◽  
Angiotensin System ◽  
Uncontrolled Diabetes ◽  
Receptor Blockers

Volume depletion due to persistent glucosuria-induced osmotic diuresis is a significant problem in uncontrolled diabetes mellitus (DM). Angiotensin II receptor blockers (ARBs), such as candesartan, slow the progression of chronic kidney disease in patients with DM. However, mice with genetic knockout of components of the renin-angiotensin system have urine concentrating defects, suggesting that ARBs may exacerbate the volume depletion. Therefore, the effect of candesartan on UT-A1, UT-A3, NKCC2, and aquaporin-2 (AQP2) protein abundances was determined in control and 3-wk DM rats. Aldosterone levels in control rats (0.36 ± 0.06 nM) and candesartan-treated rats (0.34 ± 0.14 nM) were the same. DM rats had higher aldosterone levels (1.48 ± 0.37 nM) that were decreased by candesartan (0.97 ± 0.26 nM). Western analysis showed that UT-A1 expression was increased in DM rats compared with controls in inner medullary (IM) tip (158 ± 13%) and base (120 ± 25%). UT-A3 abundance was increased in IM tip (123 ± 11%) and base (146 ± 17%) of DM rats vs. controls. UT-A3 was unchanged in candesartan-treated control rats. In candesartan-treated DM rats, UT-A3 increased in IM tip (160 ± 14%) and base (210 ± 19%). Candesartan-treated DM rats had slightly higher AQP2 in IM (46%, P < 0.05) vs. control rats. NKCC2/BSC1 was increased 145 ± 10% in outer medulla of DM vs. control rats. We conclude that candesartan augments compensatory changes in medullary transport proteins, reducing the losses of solute and water during uncontrolled DM. These changes may represent a previously unrecognized beneficial effect of type 1 ARBs in DM.

scholarly journals Increased phosphorylation of focal adhesion kinase in diabetic rat kidney glomeruli

Diabetologia ◽  
1995 ◽  
Vol 38 (10) ◽  
pp. 1131-1137 ◽  
Author(s):  
S. Clark ◽  
N. La Greca ◽  
M. E. Dunlop ◽  
E. Muggli
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Rat Kidney ◽  
Diabetic Rat

Abstract P184: Co-localization and Natriuretic Interdependence of Angiotensin AT2R and MasR in Obese Rat Kidney

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sanket N Patel ◽  
Quaisar Ali ◽  
Ulrike Muscha Steckelings ◽  
Tahir Hussain
Keyword(s):  
Rat Kidney ◽  
Sulfhydryl Groups ◽  
Zucker Rats ◽  
Diabetic Rat ◽  
Physical Interaction ◽  
Potential Mechanism ◽  
Obese Rats ◽  
Obese Zucker Rats ◽  
Made In

The actions of angiotensin II type 2 receptor (AT 2 R) and receptor mas (MasR) are complex but show similar pro-natriuretic function; particularly AT 2 R expression and natriuretic function are enhanced in obese/diabetic rat kidney. In light of previous reports, we tested hypothesis that AT 2 R and MasR are interdependent to produce natriuresis in obese rats due to potential physical interaction. Infusion of AT 2 R agonist C21 (5 μg/kg/min) in obese Zucker rats (OZR) caused diuresis/natriuresis which were attenuated by simultaneous infusion of the AT 2 R antagonist PD123319 (50 μg/kg/min) or the MasR antagonist A-779 (50 μg/kg/min). Similarly, infusion of MasR agonist Ang-(1-7) (110 fmol/kg/min) in OZR caused diuresis/netriuresis, which were attenuated by simultaneous infusion of A-779 or PD123319. Dual labeling of AT 2 R and MasR in OZR kidney slices revealed four-fold co-localization of AT 2 R and MasR (9.83 vs. 2.50 dual labeled cells/1600 μm 2 ) compared with lean rats in which AT 2 R is not natriuretic. Moreover, the AT 2 R co-immunoprecipitates with MasR in cortical homogenate of OZR. Immunoblotting of AT 2 R and MasR with zero length oxidative (sulfhydryl groups) cross-linker cupric-phenanthroline in OZR cortical homogenate revealed a shift of AT 2 R (~62 kDa) and MasR (~54 kDa) bands upward with overlapping migration for their complexes (~160 kDa and 245 kDa) which were sensitive to the reducing β-mercaptoethanol. Similar observations were made in HK-2 cells, where glucose (25 mM) treatment enhanced the crosslinking. Collectively, the study reveals AT2R and MasR are co-localized and functionally interdependent in producing natriuretic response. Hyperglycemic oxidative stress affecting sulfhydryl groups present a potential mechanism of such physical interaction between these receptors. (Support: R01DK061578)

scholarly journals Changes in Facilitative Glucose Transporter Messenger Ribonucleic Acid Levels in the Diabetic Rat Kidney*

Endocrinology ◽  
1997 ◽  
Vol 138 (3) ◽  
pp. 1267-1275 ◽  
Author(s):  
Edward Chin ◽  
A. Musa Zamah ◽  
Daniel Landau ◽  
Henning Gronboek ◽  
Allan Flyvbjerg ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Glucose Transporter ◽  
Rat Kidney ◽  
Diabetic Rat ◽  
Mrna Levels ◽  
Messenger Rnas ◽  
Early Diabetes ◽  
Messenger Ribonucleic Acid ◽  
Nephron Segment ◽  
Facilitative Glucose Transporter

Abstract Facilitative glucose transporter (GLUTs 1, 2, 4, and 5) messenger RNAs (mRNAs) are differentially distributed in the rat nephron: GLUT1 is widely expressed, GLUT4 is selectively concentrated in thick ascending limbs, and GLUT2 and 5 are exclusively localized in proximal tubules, consistent with differential roles for these transporters in renal glucose handling. In the present study, quantitative in situ hybridization was used to evaluate changes in these mRNA levels during acute (2 and 7 days) and chronic (30, 90, and 180 days) streptozotocin-induced diabetes mellitus (STZ-DM). Medullary GLUT1 and GLUT4 mRNA levels were significantly increased during the acute phase but returned to normal after 1 week. Cortical GLUT1 mRNA levels, however, were decreased significantly from 7 days through 6 months of STZ-DM. Cortical GLUT2 mRNA was slightly increased acutely and increased 5-fold in chronic STZ-DM, with the largest increase focally concentrated in the convoluted portion of the proximal tubule. Proximal tubule GLUT5 mRNA levels also were increased significantly during chronic STZ-DM. In summary, medullary GLUT1 and GLUT4 mRNA levels are acutely increased in STZ-DM, paralleling the increased renal epithelial metabolic activity accompanying early diabetes. Proximal tubular GLUT2 and 5 mRNA levels were increased in chronic STZ-DM, possibly adapting to the increased need for glucose transport out of these epithelial cells, whereas the concomitant decrease in cortical GLUT1 expression may reflect the decreased requirement for basolateral import of glucose into these same cells. Thus, renal GLUTs demonstrate complex, nephron segment-specific and duration-dependent responses to the effects of STZ-DM.

scholarly journals AQP1 expression in the proximal tubule of diabetic rat kidney

Heliyon ◽  
2020 ◽  
Vol 6 (1) ◽  
pp. e03192
Author(s):  
Erika A. Seyahian ◽  
Leornardo Cacciagiu ◽  
Alicia E. Damiano ◽  
Elsa Zotta
Keyword(s):  
Proximal Tubule ◽  
Rat Kidney ◽  
Diabetic Rat ◽  
Aqp1 Expression

scholarly journals Proteomic Analysis of Protease Resistant Proteins in the Diabetic Rat Kidney

2012 ◽  
Vol 12 (1) ◽  
pp. 228-236 ◽  
Author(s):  
Sneha B. Bansode ◽  
Ashok D. Chougale ◽  
Rakesh S. Joshi ◽  
Ashok P. Giri ◽  
Subhash L. Bodhankar ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Rat Kidney ◽  
Diabetic Rat

scholarly journals Human munc13 Is a Diacylglycerol Receptor that Induces Apoptosis and May Contribute to Renal Cell Injury in Hyperglycemia

1999 ◽  
Vol 10 (5) ◽  
pp. 1609-1619 ◽  
Author(s):  
Yong Song ◽  
Menachem Ailenberg ◽  
Mel Silverman
Keyword(s):  
Phorbol Ester ◽  
Renal Cell ◽  
Cell Injury ◽  
Rat Kidney ◽  
Diabetic Rat ◽  
Opossum Kidney ◽  
Opossum Kidney Cells ◽  
Renal Cell Line ◽  
Diabetic Rat Model

We have previously shown that human munc13 (hmunc13) is up-regulated by hyperglycemia under in vitro conditions in human mesangial cell cultures. The purpose of the present study was to determine the cellular function of hmunc13. To do this, we have investigated the subcellular localization of hmunc13 in a transiently transfected renal cell line, opossum kidney cells. We have found that hmunc13 is a cytoplasmic protein and is translocated to the Golgi apparatus after phorbol ester stimulation. In addition, cells transfected with hmunc13 demonstrate apoptosis after treatment with phorbol ester, but cells transfected with an hmunc13 deletion mutant in which the diacylglycerol (C1) binding domain is absent exhibit no change in intracellular distribution and no induction of apoptosis in the presence of phorbol ester stimulation. We conclude that both the diacylglycerol-induced translocation and the apoptosis represent functional activity of hmunc13. We have also demonstrated that munc13-1 and munc13-2 are localized mainly to cortical epithelial cells in rat kidney and both are overexpressed under conditions of hyperglycemia in a streptozotocin-treated diabetic rat model. Taken together, our data suggest that hmunc13 serves as a diacylglycerol-activated, PKC-independent signaling pathway capable of inducing apoptosis and that this pathway may contribute to the renal cell complications of hyperglycemia.

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