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Systemic Klotho therapy protects against insulitis and enhances beta-cell mass in NOD mice.

Abstract：

:The levels of the anti-aging protein α-Klotho, in its soluble form (s-Klotho), are depressed in the circulation of patients with type 1 diabetes (T1D) or type 2 diabetes (T2D). Gene transfer experiments have suggested a protective role for β-cell specific expression of α-Klotho in murine models of T1D and T1D, but these approaches are not easily translatable to clinical therapy. It is unknown whether systemic s-Klotho protein treatment ameliorates disease in T1D, which is characterized by autoimmune destruction of β cells. We previously reported from in vitro experiments with β cells that s-Klotho increases insulin secretion, reduces cells death and promotes β-cell replication. Here, we investigated s-Klotho protein therapy in NOD mice, which have autoimmune T1D. We observed that diabetic NOD mice have significantly lower plasma levels of s-Klotho, compared to their non-diabetic counterparts. To examine in vivo effects of Klotho, we treated NOD mice with s-Klotho protein, or with a Klotho blocking antibody. Systemic treatment with s-Klotho ameliorated diabetes; notably increasing β-cell replication and total β-cell mass. Klotho expression was increased locally in the islets. s-Klotho also markedly reduced immune-cell infiltration of islets (insulitis). In contrast, administration of the Klotho antibody was detrimental, and aggravated the loss of β-cell mass. Thus, s-Klotho has protective effects in this model of T1D, and this appears to depend on a combination of increased β-cell replication and reduced insulitis. These findings suggest that s-Klotho might be effective as a new therapeutic agent for T1D.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Prud'homme GJ,Glinka Y,Kurt M,Liu W,Wang Q

doi

10.1016/j.bbrc.2020.02.123

subject

Has Abstract

pub_date

2020-05-07 00:00:00

pages

693-698

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)30404-6

journal_volume

525

pub_type

杂志文章

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