scholarly journals Physiological and Pathological Functions of SLC26A6

2021 ◽  
Vol 7 ◽  
Author(s):  
Juan Wang ◽  
Wenkang Wang ◽  
Hui Wang ◽  
Biguang Tuo
Keyword(s):  
Ion Homeostasis ◽  
Acid Base Balance ◽  
Acid Base ◽  
The Past ◽  
Anion Transporter ◽  
Transporter Family ◽  
Base Balance ◽  
Extensive Exchange ◽  
Solute Carrier

Solute Carrier Family 26 (SLC26) is a conserved anion transporter family with 10 members in human (SLC26A1-A11, A10 being a pseudogene). All SLC26 genes except for SLC26A5 (prestin) are versatile anion exchangers with notable ability to transport a variety of anions. SLC26A6 has the most extensive exchange functions in the SLC26 family and is widely expressed in various organs and tissues of mammals. SLC26A6 has some special properties that make it play a particularly important role in ion homeostasis and acid-base balance. In the past few years, the function of SLC26A6 in the diseases has received increasing attention. SLC26A6 not only participates in the development of intestinal and pancreatic diseases but also serves a significant role in mediating nephrolithiasis, fetal skeletal dysplasia and arrhythmia. This review aims to explore the role of SLC26A6 in physiology and pathophysiology of relative mammalian organs to guide in-depth studies about related diseases of human.

DUNCAN'S DISEASES OF METABOLISM: ENDOCRINOLOGY, ed 7. Edited by Philip K. Bondy and Leon E. Rosenberg. Philadelphia, WB Saunders Co, 1974, $26; 736 pp

PEDIATRICS ◽  
1977 ◽  
Vol 59 (5) ◽  
pp. 794-794
Author(s):  
Lester F. Soyka
Keyword(s):  
Clinical Endocrinology ◽  
Normal Structure ◽  
Acid Base Balance ◽  
Acid Base ◽  
Telephone Directory ◽  
The Past ◽  
Big City ◽  
Recent Developments ◽  
Base Balance ◽  
And Function

The endocrinology section of Duncan's Diseases of Metabolism comprises 736 pages, or about 44% of the total text. The division of this seventh edition of a classic text in the field is perhaps a logical expression of the splitting of endocrinology from metabolism as each field has grown tremendously in the past decade. The endocrinology portion is compact and easy to use because of this division, aided by the employment of thin, though substantial paper and small, but easily readable type. These combine to avoid the feeling of consulting a big-city telephone directory, which is so common with use of many of the standard textbooks of today. The illustrations are generally excellent and the 54-page index, which covers both sections of the book, is unusually thorough. As in all textbooks, many sections are outdated before they appear in print. Although the editors, Philip K. Bondy and Leon E. Rosenberg, propose to avoid this by means of a "last-minute" addendum, only two of the 13 chapters bear such, and one of these lists only three references, all dating to 1972. The other recent-developments section is longer and more helpful. The content is essentially that of general clinical endocrinology, each chapter using the standard approach of considering normal structure and function and then diseases in a gland arrangement, starting with the hypothalamus and traveling downward to the testis and ovary. A small chapter on acid-base balance seems out of place, whereas those on nonendocrine-secreting tumors and serotonin and the carcinoid syndrome are useful extensions of the scope of endocrinology.

Role of organic anions in renal response to dietary acid and base loads

1989 ◽  
Vol 257 (2) ◽  
pp. F170-F176 ◽  
Author(s):  
J. C. Brown ◽  
R. K. Packer ◽  
M. A. Knepper
Keyword(s):  
Organic Anion ◽  
Organic Anions ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Urine Ph ◽  
Renal Response ◽  
Base Balance ◽  
Net Acid Excretion

Bicarbonate is formed when organic anions are oxidized systemically. Therefore, changes in organic anion excretion can affect systemic acid-base balance. To assess the role of organic anions in urinary acid-base excretion, we measured urinary excretion in control rats, NaHCO3-loaded rats, and NH4Cl-loaded rats. Total organic anions were measured by the titration method of Van Slyke. As expected, NaHCO3 loading increased urine pH and decreased net acid excretion (NH4+ + titratable acid - HCO3-), whereas NH4Cl loading had the opposite effect. Organic anion excretion was increased in response to NaHCO3 loading and decreased in response to NH4Cl loading. We quantified the overall effect of organic ion plus inorganic buffer ion excretion on acid-base balance. The amounts of organic anions excreted by all animals in this study were greater than the amounts of NH4+, HCO3-, or titratable acidity excreted. In addition, in response to acid and alkali loading, changes in urinary organic anion excretion were 40-50% as large as changes in net acid excretion. We conclude that, in rats, regulation of organic anion excretion can contribute importantly to the overall renal response to acid-base disturbances.

Decrease in ureagenesis by partial hepatectomy does not influence acid-base balance

1989 ◽  
Vol 257 (4) ◽  
pp. F696-F699
Author(s):  
T. Almdal ◽  
H. Vilstrup ◽  
K. Bjerrum ◽  
L. O. Kristensen
Keyword(s):  
Sodium Chloride ◽  
Sodium Bicarbonate ◽  
Synthesis Rate ◽  
Urea Synthesis ◽  
Ph Homeostasis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Bicarbonate Infusion

It has been suggested that urea synthesis participates directly in body pH homeostasis by removal of bicarbonate. To elucidate this hypothesis sodium bicarbonate or sodium chloride was infused (11.5 mumol/min) for 90 min into control rats and into rats that had undergone an 85% hepatectomy immediately before starting the infusion. Urea synthesis rate was 2.6 +/- 0.3 mumol/min (mean +/- SE) in controls, and was significantly (P less than 0.01) reduced to 1.0 +/- 0.2 mumol/min in partially hepatectomized rats. At the start of bicarbonate infusion, pH was 7.38 and 7.34 in control and partially hepatectomized rats, respectively, and at the end of infusion, pH was 7.56 and 7.51. Standard bicarbonate at start of bicarbonate infusion was 21.9 and 21.3 mM in controls and partially hepatectomized, respectively, and it increased to 32.7 and 29.9 mM at end of infusion. In saline-infused rats a slight decrease of approximately 0.05 pH units was observed during the experiment, but again no difference emerged between control and partially hepatectomized rats. It is concluded that a major role of the liver in the regulation of acid-base balance is unlikely.

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