For several years I have blogged about the kidney "smelling" stuff. Shepard and Pluznick have now updated their work on kidney olfactory receptor 1393 and it's role in diabetic nephropathy. In mice with this receptor knocked-out, Sglt1 is reduced in the proximal tubular lumen, This results in glycosuria with improvement in glucose tolerance.
They then took these mice and fed them a high fat diet. Even with the development of obesity, the knock-out mice maintained better glucose tolerance and did not develop an elevated glomerular filtration rate as wild-type counterparts did. Insulin tolerance was similar between the groups. Mice lacking the olfactory receptor also accumulated less fat in the liver than their wild-type brethren, even though body weights were similar.
There's still more to learn from these animals, but this is exciting work for sure!
This year, we also learned that kidneys can taste! Sweet receptors have been found in the pancreas and other areas of the gut beyond the tongue. They can regulate function of these organs in response to sugars and artificial sweeteners. Kassem, Ares, and Ortiz now show that sweet receptors T1R2/T1R3 are present in the kidney! They localize to the thick ascending limb and increase the presence of NKCC2 on the surface in response to fructose feeding. Gumarin, an antagonist of the receptor, blocks this response to fructose. The knock-out mouse for this sweet receptor shows diminished levels of NKCC2 in the tubular surface; these mice also have increased urine output with decreased osmolality, consistent with diminished efficiency of loop function.
The study only addressed effects of fructose, but given interactions of artificial sweeteners in the gut, there will be a lot more exciting information coming up, I'm sure.
The kidney: it tastes, it smells, it pees. Makes you think twice about eating that asparagus, huh?
Abstracts linked to author names above.