5-Aminolevulinic acid with ferrous iron improves early renal damage and hepatic steatosis in high fat diet-induced obese mice.

5-aminolevulinic acid diabetic nephropathy heme oxygenase-1 hepatic steatosis high fat diet

Journal

Journal of clinical biochemistry and nutrition
ISSN: 0912-0009
Titre abrégé: J Clin Biochem Nutr
Pays: Japan
ID NLM: 8700907

Informations de publication

Date de publication:
Jan 2019
Historique:
received: 15 03 2018
accepted: 11 06 2018
entrez: 2 2 2019
pubmed: 2 2 2019
medline: 2 2 2019
Statut: ppublish

Résumé

5-Aminolevulinic acid, a natural amino acid, activates mitochondrial respiration and induces heme oxygenase-1 expression. Obesity and type 2 diabetes mellitus are associated with age-related mitochondrial respiration defect, oxidative stress and inflammation. The aim of this study is to investigate the effects of 5-aminolevulinic acid with sodium ferrous citrate on early renal damage and hepatic steatosis. 7-Month-old C57BL/6 mice were fed with a standard diet or high fat diet for 9 weeks, which were orally administered 300 mg/kg 5-aminolevulinic acid combined with 47 mg/kg sodium ferrous citrate (5-aminolevulinic acid/sodium ferrous citrate) or vehicle for the last 5 weeks. We observed that 5-aminolevulinic acid/sodium ferrous citrate significantly decreased body weight, fat weight, hepatic lipid deposits and improved levels of blood glucose and oral glucose tolerance test. In addition, 5-aminolevulinic acid/sodium ferrous citrate suppressed increased glomerular tuft area in high fat diet-fed mice, which was associated with increased heme oxygenase-1 protein expression. Our findings demonstrate additional evidence that 5-aminolevulinic acid/sodium ferrous citrate could improve glucose and lipid metabolism in diabetic mice. 5-Aminolevulinic acid/sodium ferrous citrate has potential application in obesity or type 2 diabetes mellitus-associated disease such as diabetic nephropathy and nonalcoholic fatty liver disease.

Identifiants

pubmed: 30705513
doi: 10.3164/jcbn.18-35
pii: jcbn18-35
pmc: PMC6348406
doi:

Types de publication

Journal Article

Langues

eng

Pagination

59-65

Déclaration de conflit d'intérêts

The authors declare that they have no competing interest. A. Kamiya, T. Hara, Y. Kuroda, U. Ota, M. Ishizuka, M. Nakajima, T. Tanaka are employees of SBI Pharmaceuticals Co., Ltd.

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Auteurs

Atsuko Kamiya (A)

SBI Pharmaceuticals Co. Ltd., 1-6-1 Roppongi, Minato-ku, Tokyo 106-6020, Japan.

Takeshi Hara (T)

SBI Pharmaceuticals Co. Ltd., 1-6-1 Roppongi, Minato-ku, Tokyo 106-6020, Japan.

Masayuki Tsuda (M)

Institute for Laboratory Animal Research, Kochi Medical School, Kohasu, Oko, Nankoku, Kochi 783-8505, Japan.

Emi Tsuru (E)

Institute for Laboratory Animal Research, Kochi Medical School, Kohasu, Oko, Nankoku, Kochi 783-8505, Japan.

Yasushi Kuroda (Y)

SBI Pharmaceuticals Co. Ltd., 1-6-1 Roppongi, Minato-ku, Tokyo 106-6020, Japan.

Urara Ota (U)

SBI Pharmaceuticals Co. Ltd., 1-6-1 Roppongi, Minato-ku, Tokyo 106-6020, Japan.

Takashi Karashima (T)

Department of Urology, Kochi Medical School, Kohasu, Oko, Nankoku, Kochi 783-8505, Japan.

Hideo Fukuhara (H)

Department of Urology, Kochi Medical School, Kohasu, Oko, Nankoku, Kochi 783-8505, Japan.

Keiji Inoue (K)

Department of Urology, Kochi Medical School, Kohasu, Oko, Nankoku, Kochi 783-8505, Japan.

Masahiro Ishizuka (M)

SBI Pharmaceuticals Co. Ltd., 1-6-1 Roppongi, Minato-ku, Tokyo 106-6020, Japan.

Motowo Nakajima (M)

SBI Pharmaceuticals Co. Ltd., 1-6-1 Roppongi, Minato-ku, Tokyo 106-6020, Japan.

Tohru Tanaka (T)

SBI Pharmaceuticals Co. Ltd., 1-6-1 Roppongi, Minato-ku, Tokyo 106-6020, Japan.

Classifications MeSH