Plasma leptin concentrations are associated with bone mineral density and the presence of vertebral fractures in postmenopausal women

Yamauchi, Mika; Sugimoto, Toshitsugu; Yamaguchi, Toru; Nakaoka, Daiki; Kanzawa, Michiko; Yano, Shozo; Ozuru, Rieko; Sugishita, Takeshi; Chihara, Kazuo

doi:10.1046/j.1365-2265.2001.01361.x

Cited by 200 publications

(131 citation statements)

References 29 publications

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“…This relationship was observed even in young patients with recent onset type 1 diabetes, leading to the hypothesis that insulin is a cornerstone of bone anabolic factor 28) . Also, Streptozocin-induced diabetic , while some showed negative correlations 19,20) . Likewise, consensus on the leptin-BMD relationship is not achieved in diabetic patients.…”

Section: Resultsmentioning

confidence: 98%

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Leptin is Negatively Associated with Femoral Bone Mineral Density in Postmenopausal Women with Type 2 Diabetes Mellitus

et al. 2009

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Background: Serum leptin level and bone mineral density (BMD) are widely assumed to be positively associated with body fat mass. Numerous attempts have been made to document the relationship between leptin and BMD, but the results are inconsistent, especially in diabetic patients. Methods:A total of 60 Korean postmenopausal women with type 2 diabetes mellitus were included in the present study. The BMDs of lumbar spines (L1 to L4) and proximal femurs (trochanter, neck, and total) were measured by dual-energy X-ray absorptiometry (DXA), and biochemical markers including leptin, HbA1c, C-peptide and urine albumin-creatinine ratio (ACR) were measured for each patient. Results:Negative associations between leptin and BMD of femoral neck, trochanter, and total femur in postmenopausal women with type 2 diabetes mellitus were documented in a model adjusted for age, body fat mass, and fasting insulin level (r = -0.308, P = 0.020 and r = -0.303, P = 0.025 and r = -0.290, P = 0.032 respectively). Multiple linear regression analysis was performed revealing negative associations between leptin and BMD of the femoral neck (β = -0.369), trochanter (β = -0.324), and total femur (β = -0.317). Conclusion

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Section: Resultsmentioning

confidence: 98%

“…More recent clinical trial showed that plasma leptin levels are associated with BMD and the presence of vertebral fractures in postmenopausal women 19) .…”

Section: Introductionmentioning

confidence: 99%

Leptin is Negatively Associated with Femoral Bone Mineral Density in Postmenopausal Women with Type 2 Diabetes Mellitus

et al. 2009

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“…There are studies where a positive association has been found between leptin and BMD (14,23) while there are also studies reporting no significant association (8,24) or a negative association (13,25) Yamauchi et al (26) claimed that there is a relation between low plasma leptin levels and vertebral fractures in postmenapousal women and thus circulating leptin might play a physiological role in improving bone mass quality. Unsurprisingly, insulin values of the patients were significantly higher than controls, independent of gender.…”

Section: Discussionmentioning

confidence: 99%

Association between serum leptin level and osteoporosis in patients with type 2 diabetes mellitus

Demi̇r¹,

Gültürk²,

Özdemir³

et al. 2013

Basic Clin Sci

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Aim: As osteoporosis and diabetes mellitus are widespread diseases, it is an important question whether leptin plays a role in bone physiology or not. In this study, we aimed to investigate the relationship between serum leptin level, diabetes and osteoporosis. Methods: The present study was conducted on 49 healthy individuals and 77 patients with type 2 Diabetes mellitus (DM), a total of 126 individuals, between 40 and 60 of ages. Between 08-10 hours in the morning, venous blood samples of 15 mL were drawn from forearm veins of the individuals and transferred into concerned test tubes. After blood samples were taken, Bioelectrical Impedance Analysis (BIA) was performed. Bone mineral density (BMD) was measured by DEXA (Dual energy X-ray absorptiometry) at L 1-4 (anterior-posterior) and femur. Student t test and correlation analysis were used for the statistical analysis in the study. Results: Leptin level of women in both groups were significantly higher than those of men in both groups (p<0.05). BMD values of men in patient group was significantly lower compared to those of men in control group (p<0.05). Similarly, BMD values of women in patient group was significantly lower compared to those of women in control group (p<0.05). A positive correlation was found

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“…These favorable bone effects also were observed in vivo because leptin administration increased bone mass in estrogen-deficient rodents, (30) and circulating leptin was positively associated with bone mass in pre-and postmenopausal women. (31)(32)(33) The relative contribution of leptin-mediated secretion of FGF-23 and renal handling of 1,25(OH) 2 D 3 and phosphate in the overall effects of leptin on bone is yet unclear but probably represents only a small part of the overall picture. Indeed, we still do not understand the mechanistic processes that positively link overweight (not true obesity) with bone mass and reduced fracture risk.…”

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confidence: 99%

The white adipose tissue connection with calcium and bone homeostasis

Bouillon

Decallonne

2010

Journal of Bone and Mineral Research

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T he idea of fat cells and tissue being the passive storage site of excess energy has long been gone. Not surprisingly, fat cells (white adipose tissue) were first recognized as being the source of hormones controlling energy homeostasis because they secrete more leptin with increasing fat stores. (1) Leptin then crosses the blood-brain barrier to activate its receptor in the hypothalamic regions, thereby starting a complex feedback on energy intake and expenditure but also regulating other systems such as sexual maturation and reproduction (2) and bone homeostasis. (3) Indeed, a series of elegant studies of the Karsenty group clearly demonstrated that central activation of leptin signaling activates the sympathetic postganglionic neuronal system that ultimately decreases bone formation and increases bone resorption. (3,4) Leptin receptors are also found outside the hypothalamus in insulin-producing b cells, bone marrow stromal cells, osteoblasts and chondrocytes, and kidney cells. (5) This suggests a much wider spectrum of activities for this fat cell signal, not mediated by a central neuroendocrine system.A few years ago, Horiuchi's laboratory (6,7) described increased serum concentrations of 1,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ], calcium, and phosphate in leptin-deficient (ob/ob) mice owing to increased renal expression of CYP27B1 [¼ 25(OH)D 1a-hydroxylase] that could be corrected by intraperitoneal leptin injections. The same group (8) now expands this observation by demonstrating that leptin stimulates the osteoblast (osteocyte?) production of fibroblast growth factor 23 (FGF-23), which is thereafter responsible for the downregulation of CYP27B1 and of the sodium-phosphate cotransporters (NaPT-II). The overproduction of 1,25(OH) 2 D 3 also was present in mice with leptin receptor deficiency (db/db mice) but could not, in contrast to the ob/ob mice, be corrected by intraperitoneal leptin injection. FGF-23 therapy also corrected the overproduction of 1,25(OH) 2 D 3 in ob/ob mice (not reported for db/db mice). Addition of leptin to renal tubular cell cultures did not modify the local 1a-hydroxylase activity. (8) clearly demonstrating the indirect effects of leptin.What Are the Implications of These Observations?F irst, the new data further elucidate the complex regulation of the renal production of the vitamin D hormone. Indeed, it is now well established that calcium/calcium sensing receptordriven parathyroid hormone (PTH) secretion constitutes the major stimulus for renal 1a-hydroxylase and thus the production of systemic 1,25(OH) 2 D 3 while shutting down the expected renal activation of CYP24A1, the major degradation system for vitamin D metabolites. (9)(10)(11) The second systemic hormone, osteocytic FGF-23, is a negative regulator of renal 1a-hydroxylase activity, whereas both PTH and FGF-23 decrease the tubular reabsorption of phosphate by downregulation of NaPT-II. The PTH and FGF-23 hormones thus regulate vitamin D activation, as driven by calcium and phosphate, respectively (12)(13)(14) (Fig. 1...

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Plasma leptin concentrations are associated with bone mineral density and the presence of vertebral fractures in postmenopausal women

Abstract: Our study showed that plasma leptin levels but not %fat are associated with BMD and the presence of vertebral fractures in postmenopausal women, suggesting that circulating leptin might play a physiological role in maintaining bone mass as well as better bone quality.

Cited by 200 publications

References 29 publications

Leptin is Negatively Associated with Femoral Bone Mineral Density in Postmenopausal Women with Type 2 Diabetes Mellitus

Leptin is Negatively Associated with Femoral Bone Mineral Density in Postmenopausal Women with Type 2 Diabetes Mellitus

Association between serum leptin level and osteoporosis in patients with type 2 diabetes mellitus

The white adipose tissue connection with calcium and bone homeostasis

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