Acidic Sialidase Activity Is Aberrant in Obese and Diabetic Mice

Mammalian sialidases (NEU1, NEU2, NEU3 and NEU4) that remove sialic acids from glycoconjugates have been implicated in diverse cellular functions. Human sialidases are involved in the development of various disease states such as cancer, diabetes and arteriosclerosis. Unregulated acidic sialidase NE...

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Bibliographic Details
Published in:Biological & pharmaceutical bulletin 2013/06/01, Vol.36(6), pp.1027-1031
Main Authors: Natori, Yujin, Ohkura, Naoki, Nasui, Miwako, Atsumi, Gen-ichi, Kihara-Negishi, Fumiko
Format: Article
Language:English
Subjects:
3T3-L1 Cells
Adipose Tissue - metabolism
Animals
db/db mouse
Diabetes Mellitus - metabolism
Epididymis - metabolism
fat
Kidney - metabolism
liver
Liver - metabolism
Male
Mice
Mice, Transgenic
Neuraminidase - genetics
Neuraminidase - metabolism
obesity
Obesity - metabolism
RNA, Messenger - metabolism
RNA, Small Interfering - administration & dosage
sialidase
Tsumura Suzuki Obese Diabetes mouse
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Summary:Mammalian sialidases (NEU1, NEU2, NEU3 and NEU4) that remove sialic acids from glycoconjugates have been implicated in diverse cellular functions. Human sialidases are involved in the development of various disease states such as cancer, diabetes and arteriosclerosis. Unregulated acidic sialidase NEU1 activity is associated with the pathogenesis of lysosomal storage disorder (LSD) sialidosis, abnormal immune responses and cancer progression. Obesity is closely related to several chronic diseases such as diabetes, cardiovascular diseases, hyperlipidemia or hypertension that are associated with metabolic syndrome. We examined fluctuations in mRNA levels and sialidase activities of NEU1 in two strains of obese and diabetic mice to assess the involvement of NEU1 in obesity. The activity of NEU1 was preferentially higher in epididymal fat and lower in the livers of two strains of obese and diabetic mice. Fluctuations in NEU1 activity might be associated with the pathological status of these tissues in obesity.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.b12-00995