Circulating leptin and ghrelin are differentially influenced by estrogen/progestin therapy and raloxifene

Lambrinoudaki, Ιrene; Christodoulakos, George; Economou, Emmanuel; Vlachou, Sofia; Panoulis, Constantinos; Alexandrou, Andreas; Kouskouni, Evangelia; Creatsas, George

doi:10.1016/j.maturitas.2007.10.003

Cited by 23 publications

(27 citation statements)

References 73 publications

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“…Thus, it is not surprising that leptin or Lepr signaling (the key negative regulatory hormone for body fat (42)) also plays a negative regulatory role in bone responsiveness to mechanical loading. More importantly, the findings that 1) the increase in obesity in postmenopausal women is associated with an increase in the circulating leptin level (43), 2) estrogen replacement in post- menopausal women decreases serum leptin levels (44), and 3) the PvuII and XbaI polymorphisms of ER␣ significantly influence the association between the Q223R polymorphism of human LEPR and peak bone mineral density (45) raise the interesting possibility that the suppressive action of leptin or Lepr signaling on bone mechanosensitivity might also have a role in the reduction in bone formation in postmenopausal osteoporotic patients. Our future studies will address these very interesting possibilities.…”

Section: Discussionmentioning

confidence: 99%

Leptin Receptor (Lepr) Is a Negative Modulator of Bone Mechanosensitivity and Genetic Variations in Lepr May Contribute to the Differential Osteogenic Response to Mechanical Stimulation in the C57BL/6J and C3H/HeJ Pair of Mouse Strains

Kapur

Amoui

Kesavan

et al. 2010

Journal of Biological Chemistry

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This study investigated the role of leptin receptor (Lepr) signaling in determining the bone mechanosensitivity and also evaluated whether differences in the Lepr signaling may contribute to the differential osteogenic response of the C57BL/6J (B6) and C3H/HeJ (C3H) pair of mouse strains to mechanical stimuli. This study shows that a loading strain of ϳ2,500 ⑀, which was insufficient to produce a bone formation response in B6 mice, significantly increased bone formation parameters in leptin-deficient ob ؊ /ob ؊ mice and that a loading strain of ϳ3,000 ⑀ also yielded greater osteogenic responses in Genetics play a key role in determining the bone response to mechanical loading. Accordingly, C57BL/6J (B6) 2 inbred strain mice respond to in vivo loading with an increase in bone formation, but C3H/HeJ (C3H) inbred strain mice show no such response (1-4). Quantitative trait locus mapping studies of the C3H/B6 pair of mouse strains revealed that the bone mechanosensitivity is regulated by genes located in multiple quantitative trait loci on a number of chromosomes (5, 6) and that significant interactions exist among these quantitative trait loci (6). Thus, the genetic component contributing to the differential bone response to loading in the B6/C3H pair of mouse strains is complex and involves multiple genes. Studies of the identity of and interactions among these mechanosensitivity-modulating genes would yield not only information about mechanical stimulation of bone formation but also insights into the pathophysiology of various bone-wasting diseases (e.g. osteoporosis).Our previous studies, using primary osteoblasts of the C3H/B6 pair of mouse strains as an in vitro model system and fluid shear stress as an in vitro surrogate of mechanical strain (7), have disclosed two pieces of relevant information: 1) some of the genetic components determining bone mechanosensitivity in the C3H/B6 pair of mouse strains are intrinsic to osteoblasts, and 2) some of the "mechanosensitivity" genes contributing to the good and poor bone formation response in B6 and C3H mice, respectively, are upstream from four anabolic pathways (the Wnt (wingless-and Int-related protein), IGF-I, estrogen receptor (ER), and bone morphogenetic protein (BMP)/ transforming growth factor ␤ (TGF␤) pathways).Our search for candidate mechanosensitivity genes focused initially on mouse chromosome 4, because functional genetic studies indicated that at least one region in mouse chromosome 4 harbors mechanosensitivity-modulating genes. Specifically, the B6.C3H-4T congenic mouse strain, which is genetically identical to B6 except that it carried a segment of C3H chromosome 4 (between 40 and 80 centimorgans), was more respon-

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Section: Discussionmentioning

confidence: 99%

Leptin Receptor (Lepr) Is a Negative Modulator of Bone Mechanosensitivity and Genetic Variations in Lepr May Contribute to the Differential Osteogenic Response to Mechanical Stimulation in the C57BL/6J and C3H/HeJ Pair of Mouse Strains

Kapur

Amoui

Kesavan

et al. 2010

Journal of Biological Chemistry

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“…In ovariectomized rats, raloxifene treatment reversed estrogen deficiency-induced hyperleptinemia and reduced total fat mass [45]. In two clinical studies conducted in postmenopausal women, raloxifene treatment (lasting for 3 and 6 months, respectively) significantly increased serum leptin level compared to baseline [59,60]. In contrast, another study found that serum leptin levels remained unchanged compared to baseline in postmenopausal women receiving raloxifene treatment, although serum leptin levels were significantly lower in postmenopausal women receiving raloxifene compared to those receiving no treatment [61].…”

Section: The Effects Of Raloxifene On Metabolismmentioning

confidence: 97%

Effect of selective estrogen receptor modulators on metabolic homeostasis

Lovre

Mauvais-Jarvis

2016

Biochimie

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“…Precise mechanism for the discrepancy remains unknown, but may relate to the distinction of age (Matsubara et al, 2004), physiological status (Chu et al, 2006) and variation in methods used for estrogen application (Kellokoski et al, 2005;Chu et al, 2006). Estrogen replacement therapy in post-menopausal women has been reported to induce increase (Kellokoski et al, 2005;Lambrinoudaki et al, 2008), no significant change, or even decreases (Chu et al, 2006) in serum total and acyl ghrelin secretion. In female rats, ovariectomy induces a transient augment in plasma acyl ghrelin, ghrelin expressing cells and ghrelin mRNA in stomach (Matsubara et al, 2004).…”

Section: Ghrelin and Estrogenmentioning

confidence: 99%

Ghrelin, a Gastric Hormone with Diverse Functions

Li¹,

Luo²,

Li³

et al. 2012

Chemical Biology

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Circulating leptin and ghrelin are differentially influenced by estrogen/progestin therapy and raloxifene

Cited by 23 publications

References 73 publications

Leptin Receptor (Lepr) Is a Negative Modulator of Bone Mechanosensitivity and Genetic Variations in Lepr May Contribute to the Differential Osteogenic Response to Mechanical Stimulation in the C57BL/6J and C3H/HeJ Pair of Mouse Strains

Leptin Receptor (Lepr) Is a Negative Modulator of Bone Mechanosensitivity and Genetic Variations in Lepr May Contribute to the Differential Osteogenic Response to Mechanical Stimulation in the C57BL/6J and C3H/HeJ Pair of Mouse Strains

Effect of selective estrogen receptor modulators on metabolic homeostasis

Ghrelin, a Gastric Hormone with Diverse Functions

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