Blocking b-adrenergic signaling mitigates reductions in bone marrow leptin expression seen with the high calorie diet
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Purpose: We previously demonstrated the following: 1) Magnitude of bone loss and marrow adiposity induced by low calorie diet are greater than those caused by high calorie diet and 2) b-adrenergic (b-AR) blockade mitigates bone loss induced by high calorie diet and marrow adiposity induced by high calorie and low calorie diets. In the present study, we evaluated the levels of leptin in serum and bone marrow to examine whether or not b-AR blockade-induced attenuation of bone loss is associated with leptin. Materials and Methods: Male 6-week-old C57BL/6 mice were randomly assigned to one of three groups: ad-lib fed control diet (CON), high calorie diet (HIGH), and low calorie diet (LOW). In each diet group, 10 mice were treated with vehicle (VEH) while the other 10 mice were treated with propranolol, a b-AR antagonist (b-blocker; 0.5 g/L). Results: Serum leptin level was higher in HIGHVEH mice and lower in LOWVEH mice than in CONVEH mice. b-AR blockade did not alter circulating serum leptin levels, but it increased leptin secretion per unit fat mass in high calorie diet-fed mice. Both high calorie and low calorie diets decreased bone marrow leptin expression. b-AR blockade mitigated reduction of bone marrow leptin expression levels seen in mice fed high calorie diet. Conclusion: These data suggest that the b-AR signaling pathway plays a role in alteration of bone marrow adiposity in response to dietary calorie intake and that leptin is associated with b-AR-mediated regulation of bone and marrow fat.
Abstract
Purpose: We previously demonstrated the following: 1) Magnitude of bone loss and marrow adiposity induced by low calorie diet are greater than those caused by high calorie diet and 2) b-adrenergic (b-AR) blockade mitigates bone loss induced by high calorie diet and marrow adiposity induced by high calorie and low calorie diets. In the present study, we evaluated the levels of leptin in serum and bone marrow to examine whether or not b-AR blockade-induced attenuation of bone loss is associated with leptin. Materials and Methods: Male 6-week-old C57BL/6 mice were randomly assigned to one of three groups: ad-lib fed control diet (CON), high calorie diet (HIGH), and low calorie diet (LOW). In each diet group, 10 mice were treated with vehicle (VEH) while the other 10 mice were treated with propranolol, a b-AR antagonist (b-blocker; 0.5 g/L). Results: Serum leptin level was higher in HIGHVEH mice and lower in LOWVEH mice than in CONVEH mice. b-AR blockade did not alter circulating serum leptin levels, but it increased leptin secretion per unit fat mass in high calorie diet-fed mice. Both high calorie and low calorie diets decreased bone marrow leptin expression. b-AR blockade mitigated reduction of bone marrow leptin expression levels seen in mice fed high calorie diet. Conclusion: These data suggest that the b-AR signaling pathway plays a role in alteration of bone marrow adiposity in response to dietary calorie intake and that leptin is associated with b-AR-mediated regulation of bone and marrow fat.
참고문헌 (35)
- Cao JJ, "Effects of obesity on bone metabolism", J Orthop Surg Res, 6(30) (2011)
- Yaemsiri S, "Perceived weight status, overweight diagnosis, and weight control among US adults: the NHANES 2003-2008 Study", Int J Obes (Lond), 35, pp.1063~1070 (2011)
- Ihle R, "Dose-response relationships between energy availability and bone turnover in young exercising women", J Bone Miner Res, 19, pp.1231~1240 (2004)
- Ricci TA, "Calcium supplementation suppresses bone turnover during weight reduction in postmenopausal women", J Bone Miner Res, 13, pp.1045~1050 (1998)
- Riedt CS, "Overweight postmenopausal women lose bone with moderate weight reduction and 1 g", day calcium intake, 2005, pp.20, 455~463
- Bjurholm A, "Neuroendocrine peptides in bone", Int Orthop, 15, pp.325~329 (1991)
- Hohmann EL, "Innervation of periosteum and bone by sympathetic vasoactive intestinal peptide-containing nerve fibers", Science, 232, pp.868~871 (1986)
- Takeda S, "Leptin regulates bone formation via the sympathetic nervous system", Cell, 111, pp.305~317 (2002)
- Elefteriou F, "Leptin regulation of bone resorption by the sympathetic nervous system and CART", Nature, 434, pp.514~520 (2005)
- Funk D, "Role of catecholamines in the frontal cortex in the modulation of basal and stress-induced autonomic output in rats", Brain Res, 741, pp.220~229 (1996)
- Mano T, "Sympathetic neural inuence on bone metabolism in microgravity (Review)", Acta Physiol Hung, 97, pp.354~361 (2010)
- Trayhurn P, "Leptin: funda-mental aspects", Int J Obes Relat Metab Disord, 23(Suppl 1), pp.22~28 (1999)
- Zauner C, "Resting energy expenditure in short-term starvation is increased as a result of an increase in serum norepinephrine", Am J Clin Nutr, 71, pp.1511~1515 (2000)
- da Silva AA, "The role of the sympathetic nervous system in obesity-related hypertension", Curr Hypertens Rep, 11, pp.206~211 (2009)
- 백경화, "Propranolol, a β-adrenergic antagonist, attenuates the decrease in trabecular bone mass in high calorie diet fed growing mice", BMB Reports, 47(9), pp.506~511 (2014), 생화학분자생물학회
- 백경화, "Propranolol attenuates calorie restriction- and high calorie diet-induced bone marrow adiposity", BMB Reports, 47(10), pp.587~592 (2014), 생화학분자생물학회
- Ducy P, "Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass", Cell, 100, pp.197~207 (2000)
- Baek K, "Blocking β-adrenergic signaling attenuates reductions in circulating leptin, cancellous bone mass, and marrow adiposity seen with dietary energy restriction", J Appl Physiol, 113, pp.1792~1801 (1985)
- Turner RT, "Peripheral leptin regulates bone formation", J Bone Miner Res, 28, pp.22~34 (2013)
- Baek K, "Bloomfield SA: Beta-adrenergic blockade and leptin replacement e ectively mitigate disuse bone loss", J Bone Miner Res, 24, pp.792~799 (2009)
- Reseland JE, "Leptin is expressed in and secreted from primary cultures of human osteoblasts and promotes bone mineralization", J Bone Miner Res, 16, pp.1426~1433 (2001)
- Wang J, "A nutrient-sensing pathway regulates leptin gene expression in muscle and fat", Nature, 393, pp.684~688 (1998)
- Hsu SM, "Use of avidin-biotin-peroxidase complex (ABC) in immunoperoxidase techniques: a compa-rison between ABC and unlabeled antibody (PAP) procedures", J Histochem Cytochem, 29, pp.577~580 (1981)
- Van Harmelen V, "Leptin secretion from subcutaneous and visceral adipose tissue in women", Diabetes, 47, pp.913~917 (1998)
- Lönnqvist F, "Leptin secretion from adipose tissue in women. Relationship to plasma levels and gene expression", J Clin Invest, 99, pp.2398~2404 (1997)
- Couillard C, "Plasma leptin response to an epinephrine infusion in lean and obese women", Obes Res, 10, pp.6~13 (2002)
- Donahoo WT, "Isoproterenol and somatostatin decrease plasma leptin in humans: a novel mechanism regulating leptin secretion", J Clin Endocrinol Metab, 82, pp.4139~4143 (1997)
- Ricci MR, "Isoproterenol decreases leptin expression in adipose tissue of obese humans", Obes Res, 7, pp.233~240 (1999)
- Scriba D, "Catecho-lamines suppress leptin release from in vitro differentiated subcutaneous human adipocytes in primary culture via beta1- and beta2-adrenergic receptors", Eur J Endocrinol, 143, pp.439~445 (2000)
- Fain JN, "Regulation of leptin release and lipolysis by PGE2 in rat adipose tissue", Prostaglandins Other Lipid Mediat, 62, pp.343~350 (2000)
- Hoggard N, "Localization of leptin receptor mRNA splice variants in murine peripheral tissues by RT-PCR and in situ hybridization", Biochem Biophys Res Commun, 232, pp.383~387 (1997)
- Yang DC, "cAMP", PKA regulates osteogenesis, adipogenesis and ratio of RANKL, PLoS One, pp.2008, 3[DOI]
- Maymó JL, "Regulation of placental leptin expre-ssion by cyclic adenosine 5'-monophosphate involves cross talk between protein kinase A and mitogen-activated protein kinase signaling pathways", Endocrinology, 151, pp.3738~3751 (2010)
- Maeda T, "Simvastatin suppresses leptin expression in 3T3-L1 adipocytes via activation of the cyclic AMP-PKA pathway induced by inhibition of protein prenylation", J Biochem, 145, pp.771~781 (2009)
- Fain JN, "Synergism between insulin and low concentrations of isoproterenol in the stimulation of leptin release by cultured human adipose tissue", Metabolism, 49, pp.804~809 (2000)