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2016 ; 2016
(ä): 5825170
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Selective Insulin Resistance in the Kidney
#MMPMID27247938
Horita S
; Nakamura M
; Suzuki M
; Satoh N
; Suzuki A
; Seki G
Biomed Res Int
2016[]; 2016
(ä): 5825170
PMID27247938
show ga
Insulin resistance has been characterized as attenuation of insulin sensitivity
at target organs and tissues, such as muscle and fat tissues and the liver. The
insulin signaling cascade is divided into major pathways such as the PI3K/Akt
pathway and the MAPK/MEK pathway. In insulin resistance, however, these pathways
are not equally impaired. For example, in the liver, inhibition of
gluconeogenesis by the insulin receptor substrate (IRS) 2 pathway is impaired,
while lipogenesis by the IRS1 pathway is preserved, thus causing hyperglycemia
and hyperlipidemia. It has been recently suggested that selective impairment of
insulin signaling cascades in insulin resistance also occurs in the kidney. In
the renal proximal tubule, insulin signaling via IRS1 is inhibited, while insulin
signaling via IRS2 is preserved. Insulin signaling via IRS2 continues to
stimulate sodium reabsorption in the proximal tubule and causes sodium retention,
edema, and hypertension. IRS1 signaling deficiency in the proximal tubule may
impair IRS1-mediated inhibition of gluconeogenesis, which could induce
hyperglycemia by preserving glucose production. In the glomerulus, the impairment
of IRS1 signaling deteriorates the structure and function of podocyte and
endothelial cells, possibly causing diabetic nephropathy. This paper mainly
describes selective insulin resistance in the kidney, focusing on the proximal
tubule.
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