Naringin prevents bone loss in a rat model of type 1 Diabetes mellitus

M. Rivoira; V. Rodríguez; G. Picotto; R. Battaglino; N. Tolosa de Talamoni

doi:10.1016/j.abb.2017.12.001

Naringin prevents bone loss in a rat model of type 1 Diabetes mellitus

M. Rivoira, V. Rodríguez, G. Picotto, R. Battaglino, N. Tolosa de Talamoni

Research output: Contribution to journal › Article › peer-review

34 Scopus citations

Abstract

The aim of this work was to know whether naringin (NA) could prevent the bone complications in a model of streptozotocin (STZ) induced diabetes. Rats were divided in: 1) controls, 2) STZ-rats, 3) STZ-rats treated with 40 mg NA/kg, and 4) STZ-rats treated with 80 mg NA/kg. BMD and BMC were performed by DEXA. Bone histomorphometry and histology as well as TRAP staining were done in tibia. Osteocalcin (OCN) was determined in bone and serum. Glutathione content and SOD and catalase activities were assayed in bone marrow from femur. The data showed that NA80 increased the BMD and BMC from the long bones of STZ-rats. Both NA40 and NA80 normalized the trabecular number and the trabecular separations. An increase in the number of adipocytes and TRAP(+) cells in tibia from STZ-rats was blocked by NA. NA40 treatment increased the number of OCN(+) cells, but only the NA80 treatment allowed to reach the control values. NA normalized the SOD and catalase activities in bone marrow of femur from STZ-rats. In conclusion, NA avoids alterations in the physical properties and microstructure of bone from STZ-rats probably by stimulation of osteoblastogenesis, inhibition of the osteoclastogenesis and adipogenesis via blocking the oxidative stress.

Original language	English (US)
Pages (from-to)	56-63
Number of pages	8
Journal	Archives of Biochemistry and Biophysics
Volume	637
DOIs	https://doi.org/10.1016/j.abb.2017.12.001
State	Published - Jan 1 2018
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by Grants from a Bilateral Cooperation CONICET (Argentina)-National Science Foundation (USA), and Grants from CONICET (PIP 2013–2015) and SECYT (UNC), Argentina. Special thanks from the authors to GEPSA (Grupo Pilar S.A.) and the Fundación de la Facultad de Ciencias Médicas for donation of the animal diet. Prof. Dr. Nori Tolosa de Talamoni and Dr. Gabriela Picotto and Dr. Valeria Rodriguez are Members of Investigator Career from the Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET). All authors participated in the conception, design, and performance of the study as well as interpretation of data and drafting the manuscript. None of the authors had a personal conflict of interest. No conflicts of interest, financial or otherwise, are declared by the authors.

Funding Information:
This work was supported by Grants from a Bilateral Cooperation CONICET (Argentina)- National Science Foundation (USA) , and Grants from CONICET ( PIP 2013–2015 ) and SECYT (UNC) , Argentina. Special thanks from the authors to GEPSA (Grupo Pilar S.A.) and the Fundación de la Facultad de Ciencias Médicas for donation of the animal diet. Prof. Dr. Nori Tolosa de Talamoni and Dr. Gabriela Picotto and Dr. Valeria Rodriguez are Members of Investigator Career from the Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET). All authors participated in the conception, design, and performance of the study as well as interpretation of data and drafting the manuscript. None of the authors had a personal conflict of interest. No conflicts of interest, financial or otherwise, are declared by the authors.

Publisher Copyright:
© 2017 Elsevier Inc.

Keywords

Adipocytes
Bone mineral density
Naringin
Oxidative stress
TRAP(+) cells
Type 1 D.m.

PubMed: MeSH publication types

Journal Article
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, Non-U.S. Gov't

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.abb.2017.12.001

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@article{a4009bcb49954226bfa5acd0c23f948e,

title = "Naringin prevents bone loss in a rat model of type 1 Diabetes mellitus",

abstract = "The aim of this work was to know whether naringin (NA) could prevent the bone complications in a model of streptozotocin (STZ) induced diabetes. Rats were divided in: 1) controls, 2) STZ-rats, 3) STZ-rats treated with 40 mg NA/kg, and 4) STZ-rats treated with 80 mg NA/kg. BMD and BMC were performed by DEXA. Bone histomorphometry and histology as well as TRAP staining were done in tibia. Osteocalcin (OCN) was determined in bone and serum. Glutathione content and SOD and catalase activities were assayed in bone marrow from femur. The data showed that NA80 increased the BMD and BMC from the long bones of STZ-rats. Both NA40 and NA80 normalized the trabecular number and the trabecular separations. An increase in the number of adipocytes and TRAP(+) cells in tibia from STZ-rats was blocked by NA. NA40 treatment increased the number of OCN(+) cells, but only the NA80 treatment allowed to reach the control values. NA normalized the SOD and catalase activities in bone marrow of femur from STZ-rats. In conclusion, NA avoids alterations in the physical properties and microstructure of bone from STZ-rats probably by stimulation of osteoblastogenesis, inhibition of the osteoclastogenesis and adipogenesis via blocking the oxidative stress.",

keywords = "Adipocytes, Bone mineral density, Naringin, Oxidative stress, TRAP(+) cells, Type 1 D.m.",

author = "M. Rivoira and V. Rodr{\'i}guez and G. Picotto and R. Battaglino and {Tolosa de Talamoni}, N.",

note = "Funding Information: This work was supported by Grants from a Bilateral Cooperation CONICET (Argentina)-National Science Foundation (USA), and Grants from CONICET (PIP 2013–2015) and SECYT (UNC), Argentina. Special thanks from the authors to GEPSA (Grupo Pilar S.A.) and the Fundaci{\'o}n de la Facultad de Ciencias M{\'e}dicas for donation of the animal diet. Prof. Dr. Nori Tolosa de Talamoni and Dr. Gabriela Picotto and Dr. Valeria Rodriguez are Members of Investigator Career from the Consejo Nacional de Investigaciones Cient{\'i}ficas y Tecnol{\'o}gicas (CONICET). All authors participated in the conception, design, and performance of the study as well as interpretation of data and drafting the manuscript. None of the authors had a personal conflict of interest. No conflicts of interest, financial or otherwise, are declared by the authors. Funding Information: This work was supported by Grants from a Bilateral Cooperation CONICET (Argentina)- National Science Foundation (USA) , and Grants from CONICET ( PIP 2013–2015 ) and SECYT (UNC) , Argentina. Special thanks from the authors to GEPSA (Grupo Pilar S.A.) and the Fundaci{\'o}n de la Facultad de Ciencias M{\'e}dicas for donation of the animal diet. Prof. Dr. Nori Tolosa de Talamoni and Dr. Gabriela Picotto and Dr. Valeria Rodriguez are Members of Investigator Career from the Consejo Nacional de Investigaciones Cient{\'i}ficas y Tecnol{\'o}gicas (CONICET). All authors participated in the conception, design, and performance of the study as well as interpretation of data and drafting the manuscript. None of the authors had a personal conflict of interest. No conflicts of interest, financial or otherwise, are declared by the authors. Publisher Copyright: {\textcopyright} 2017 Elsevier Inc.",

year = "2018",

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doi = "10.1016/j.abb.2017.12.001",

language = "English (US)",

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T1 - Naringin prevents bone loss in a rat model of type 1 Diabetes mellitus

AU - Rivoira, M.

AU - Rodríguez, V.

AU - Picotto, G.

AU - Battaglino, R.

AU - Tolosa de Talamoni, N.

N1 - Funding Information: This work was supported by Grants from a Bilateral Cooperation CONICET (Argentina)-National Science Foundation (USA), and Grants from CONICET (PIP 2013–2015) and SECYT (UNC), Argentina. Special thanks from the authors to GEPSA (Grupo Pilar S.A.) and the Fundación de la Facultad de Ciencias Médicas for donation of the animal diet. Prof. Dr. Nori Tolosa de Talamoni and Dr. Gabriela Picotto and Dr. Valeria Rodriguez are Members of Investigator Career from the Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET). All authors participated in the conception, design, and performance of the study as well as interpretation of data and drafting the manuscript. None of the authors had a personal conflict of interest. No conflicts of interest, financial or otherwise, are declared by the authors. Funding Information: This work was supported by Grants from a Bilateral Cooperation CONICET (Argentina)- National Science Foundation (USA) , and Grants from CONICET ( PIP 2013–2015 ) and SECYT (UNC) , Argentina. Special thanks from the authors to GEPSA (Grupo Pilar S.A.) and the Fundación de la Facultad de Ciencias Médicas for donation of the animal diet. Prof. Dr. Nori Tolosa de Talamoni and Dr. Gabriela Picotto and Dr. Valeria Rodriguez are Members of Investigator Career from the Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET). All authors participated in the conception, design, and performance of the study as well as interpretation of data and drafting the manuscript. None of the authors had a personal conflict of interest. No conflicts of interest, financial or otherwise, are declared by the authors. Publisher Copyright: © 2017 Elsevier Inc.

PY - 2018/1/1

Y1 - 2018/1/1

N2 - The aim of this work was to know whether naringin (NA) could prevent the bone complications in a model of streptozotocin (STZ) induced diabetes. Rats were divided in: 1) controls, 2) STZ-rats, 3) STZ-rats treated with 40 mg NA/kg, and 4) STZ-rats treated with 80 mg NA/kg. BMD and BMC were performed by DEXA. Bone histomorphometry and histology as well as TRAP staining were done in tibia. Osteocalcin (OCN) was determined in bone and serum. Glutathione content and SOD and catalase activities were assayed in bone marrow from femur. The data showed that NA80 increased the BMD and BMC from the long bones of STZ-rats. Both NA40 and NA80 normalized the trabecular number and the trabecular separations. An increase in the number of adipocytes and TRAP(+) cells in tibia from STZ-rats was blocked by NA. NA40 treatment increased the number of OCN(+) cells, but only the NA80 treatment allowed to reach the control values. NA normalized the SOD and catalase activities in bone marrow of femur from STZ-rats. In conclusion, NA avoids alterations in the physical properties and microstructure of bone from STZ-rats probably by stimulation of osteoblastogenesis, inhibition of the osteoclastogenesis and adipogenesis via blocking the oxidative stress.

AB - The aim of this work was to know whether naringin (NA) could prevent the bone complications in a model of streptozotocin (STZ) induced diabetes. Rats were divided in: 1) controls, 2) STZ-rats, 3) STZ-rats treated with 40 mg NA/kg, and 4) STZ-rats treated with 80 mg NA/kg. BMD and BMC were performed by DEXA. Bone histomorphometry and histology as well as TRAP staining were done in tibia. Osteocalcin (OCN) was determined in bone and serum. Glutathione content and SOD and catalase activities were assayed in bone marrow from femur. The data showed that NA80 increased the BMD and BMC from the long bones of STZ-rats. Both NA40 and NA80 normalized the trabecular number and the trabecular separations. An increase in the number of adipocytes and TRAP(+) cells in tibia from STZ-rats was blocked by NA. NA40 treatment increased the number of OCN(+) cells, but only the NA80 treatment allowed to reach the control values. NA normalized the SOD and catalase activities in bone marrow of femur from STZ-rats. In conclusion, NA avoids alterations in the physical properties and microstructure of bone from STZ-rats probably by stimulation of osteoblastogenesis, inhibition of the osteoclastogenesis and adipogenesis via blocking the oxidative stress.

KW - Adipocytes

KW - Bone mineral density

KW - Naringin

KW - Oxidative stress

KW - TRAP(+) cells

KW - Type 1 D.m.

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VL - 637

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EP - 63

JO - Archives of Biochemistry and Biophysics

JF - Archives of Biochemistry and Biophysics

ER -

Naringin prevents bone loss in a rat model of type 1 Diabetes mellitus

Abstract

Bibliographical note

Keywords

PubMed: MeSH publication types

UN SDGs

Publisher link

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