Diabetes és csontanyagcsere

Translated title of the contribution: Diabetes and bone metabolism

Éva Ruzicska, G. Poór

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

In the past decade several novel findings point to the critical role of the skeleton in several homeostatic processes, including energy balance. The connection begins in the bone marrow with lineage allocation of mesenchymal stem cells to adipocytes or osteoblasts. Osteoblasts and adipocytes produce factors affecting insulin homeostasis. The hormonally active adipose tissue can regulate bone metabolism. In this review authors discuss targets taking critical part in the bone-fat network: leptin, osteocalcin, PPAR γ2 and the Wnt/beta catenin pathway. Leptin regulates energy metabolism through controlling appetite. Mutation of the leptin gene resulting leptin resistance leads to high leptin levels, enormous appetite and pathologic obesity. Leptin also can influence the bone mass. The main effects of the thiazolidinedions - PPAR γ agonists - are mediated through receptors located in adipocytes. However, beside their positive effects, they also suppress osteoblastogenesis and increase the risk for pathologic fractures. Osteocalcin, a known marker of bone formation, produced by osteoblasts decreases fat mass, promotes adiponectin production and insulin sensitivity, increases the number of pancreatic β-cells and increases insulin secretion. Thus, the skeletal system can regulate glucose metabolism and this substantially changed our view on this issue. Novel molecules can now be tested as targets in order to enhance bone formation and possibly prevent fractures.

Original languageHungarian
Pages (from-to)1156-1160
Number of pages5
JournalOrvosi Hetilap
Volume152
Issue number29
DOIs
Publication statusPublished - Jul 1 2011

Fingerprint

Leptin
Bone and Bones
Osteoblasts
Adipocytes
Peroxisome Proliferator-Activated Receptors
Osteocalcin
Appetite
Osteogenesis
Fats
Insulin
Spontaneous Fractures
Adiponectin
beta Catenin
Mesenchymal Stromal Cells
Skeleton
Energy Metabolism
Insulin Resistance
Adipose Tissue
Homeostasis
Obesity

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Diabetes és csontanyagcsere. / Ruzicska, Éva; Poór, G.

In: Orvosi Hetilap, Vol. 152, No. 29, 01.07.2011, p. 1156-1160.

Research output: Contribution to journalArticle

Ruzicska, Éva ; Poór, G. / Diabetes és csontanyagcsere. In: Orvosi Hetilap. 2011 ; Vol. 152, No. 29. pp. 1156-1160.
@article{b50b414f33714be3b13eca98f5fd8539,
title = "Diabetes {\'e}s csontanyagcsere",
abstract = "In the past decade several novel findings point to the critical role of the skeleton in several homeostatic processes, including energy balance. The connection begins in the bone marrow with lineage allocation of mesenchymal stem cells to adipocytes or osteoblasts. Osteoblasts and adipocytes produce factors affecting insulin homeostasis. The hormonally active adipose tissue can regulate bone metabolism. In this review authors discuss targets taking critical part in the bone-fat network: leptin, osteocalcin, PPAR γ2 and the Wnt/beta catenin pathway. Leptin regulates energy metabolism through controlling appetite. Mutation of the leptin gene resulting leptin resistance leads to high leptin levels, enormous appetite and pathologic obesity. Leptin also can influence the bone mass. The main effects of the thiazolidinedions - PPAR γ agonists - are mediated through receptors located in adipocytes. However, beside their positive effects, they also suppress osteoblastogenesis and increase the risk for pathologic fractures. Osteocalcin, a known marker of bone formation, produced by osteoblasts decreases fat mass, promotes adiponectin production and insulin sensitivity, increases the number of pancreatic β-cells and increases insulin secretion. Thus, the skeletal system can regulate glucose metabolism and this substantially changed our view on this issue. Novel molecules can now be tested as targets in order to enhance bone formation and possibly prevent fractures.",
keywords = "leptin, osteocalcin, PPAR 2, Wnt/beta catenin pathway",
author = "{\'E}va Ruzicska and G. Po{\'o}r",
year = "2011",
month = "7",
day = "1",
doi = "10.1556/OH.2011.29147",
language = "Hungarian",
volume = "152",
pages = "1156--1160",
journal = "Orvosi Hetilap",
issn = "0030-6002",
publisher = "Akademiai Kiado",
number = "29",

}

TY - JOUR

T1 - Diabetes és csontanyagcsere

AU - Ruzicska, Éva

AU - Poór, G.

PY - 2011/7/1

Y1 - 2011/7/1

N2 - In the past decade several novel findings point to the critical role of the skeleton in several homeostatic processes, including energy balance. The connection begins in the bone marrow with lineage allocation of mesenchymal stem cells to adipocytes or osteoblasts. Osteoblasts and adipocytes produce factors affecting insulin homeostasis. The hormonally active adipose tissue can regulate bone metabolism. In this review authors discuss targets taking critical part in the bone-fat network: leptin, osteocalcin, PPAR γ2 and the Wnt/beta catenin pathway. Leptin regulates energy metabolism through controlling appetite. Mutation of the leptin gene resulting leptin resistance leads to high leptin levels, enormous appetite and pathologic obesity. Leptin also can influence the bone mass. The main effects of the thiazolidinedions - PPAR γ agonists - are mediated through receptors located in adipocytes. However, beside their positive effects, they also suppress osteoblastogenesis and increase the risk for pathologic fractures. Osteocalcin, a known marker of bone formation, produced by osteoblasts decreases fat mass, promotes adiponectin production and insulin sensitivity, increases the number of pancreatic β-cells and increases insulin secretion. Thus, the skeletal system can regulate glucose metabolism and this substantially changed our view on this issue. Novel molecules can now be tested as targets in order to enhance bone formation and possibly prevent fractures.

AB - In the past decade several novel findings point to the critical role of the skeleton in several homeostatic processes, including energy balance. The connection begins in the bone marrow with lineage allocation of mesenchymal stem cells to adipocytes or osteoblasts. Osteoblasts and adipocytes produce factors affecting insulin homeostasis. The hormonally active adipose tissue can regulate bone metabolism. In this review authors discuss targets taking critical part in the bone-fat network: leptin, osteocalcin, PPAR γ2 and the Wnt/beta catenin pathway. Leptin regulates energy metabolism through controlling appetite. Mutation of the leptin gene resulting leptin resistance leads to high leptin levels, enormous appetite and pathologic obesity. Leptin also can influence the bone mass. The main effects of the thiazolidinedions - PPAR γ agonists - are mediated through receptors located in adipocytes. However, beside their positive effects, they also suppress osteoblastogenesis and increase the risk for pathologic fractures. Osteocalcin, a known marker of bone formation, produced by osteoblasts decreases fat mass, promotes adiponectin production and insulin sensitivity, increases the number of pancreatic β-cells and increases insulin secretion. Thus, the skeletal system can regulate glucose metabolism and this substantially changed our view on this issue. Novel molecules can now be tested as targets in order to enhance bone formation and possibly prevent fractures.

KW - leptin

KW - osteocalcin

KW - PPAR 2

KW - Wnt/beta catenin pathway

UR - http://www.scopus.com/inward/record.url?scp=79959998429&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79959998429&partnerID=8YFLogxK

U2 - 10.1556/OH.2011.29147

DO - 10.1556/OH.2011.29147

M3 - Article

VL - 152

SP - 1156

EP - 1160

JO - Orvosi Hetilap

JF - Orvosi Hetilap

SN - 0030-6002

IS - 29

ER -