Sodium butyrate improves renal injury in diabetic nephropathy through AMPK/SIRT1/PGC-1α signaling pathway

Aug 1, 2024Scientific reports

Sodium butyrate may help improve kidney damage in diabetes by activating energy and cell health pathways

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Abstract

(NaB) supplementation may improve hyperglycemia and albuminuria in mice with .

NaB treatment is associated with reduced renal tissue inflammation and extracellular matrix accumulation.
Mice receiving NaB showed decreased glomerular hypertrophy compared to controls.
NaB may alter gut microbiota composition, enhancing diversity in colonic stool.
The supplementation increased the expression of proteins related to energy metabolism and mitochondrial function, including phosphorylated AMPK and mitofusin 2.
Findings suggest that NaB could activate the in diabetic nephropathy.

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(DN) is a prototypical chronic energy metabolism imbalance disease. The plays a pivotal role in regulating energy metabolism throughout the body. Gut microbiota ferment indigestible carbohydrates to produce a variety of metabolites, particularly short-chain fatty acids (SCFAs), which exert positive effects on energy metabolism. However, the potential for SCFAs to ameliorate DN-associated renal injury via the AMPK/Sirt1/PGC-1α pathway remains a matter of debate. In this study, we investigated the effects of (NaB), a SCFA, on energy metabolism in mice with spontaneous DN at two different doses. Body weight, blood glucose and lipid levels, urinary protein excretion, liver and kidney function, interleukin-6 (IL-6) levels, and the expressions of AMPK, phosphorylated AMPK (p-AMPK), mitofusin 2 (MFN2), optic atrophy 1 (OPA1), and glucagon-like peptide-1 receptor (GLP-1R) were monitored in mice. Additionally, butyrate levels, gut microbiota composition, and diversity in colonic stool were also assessed. Our findings demonstrate that exogenous NaB supplementation can improve hyperglycemia and albuminuria, reduce renal tissue inflammation, inhibit extracellular matrix accumulation and glomerular hypertrophy, and could alter the gut microbiota composition in DN. Furthermore, NaB was found to upregulate the expressions of MFN2, OPA1, p-AMPK, and GLP-1R in DN renal tissue. These results suggest that NaB could improve the composition of gut microbiota in DN, activate the AMPK/Sirt1/PGC-1α signaling pathway, and enhance mitochondrial function to regulate energy metabolism throughout the body. Collectively, our findings indicate that NaB may be a novel therapeutic agent for the treatment of DN.

Key numbers

UACR significantly decreased in NaB1 and NaB2 groups (< 0.05)

Decrease in UACR

Comparison of UACR levels between treatment and control groups.

GLP-1 levels partially restored in NaB2 group (< 0.05)

Increase in GLP-1 levels

Serum GLP-1 levels measured after treatment.

Kidney weight reduced in NaB2 group (< 0.05)

Reduction in kidney weight

Kidney weight compared across treatment groups.

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Sodium butyrate improves renal injury in diabetic nephropathy through AMPK/SIRT1/PGC-1α signaling pathway

Abstract

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