Obesity and postmenopausal bone loss: The influence of obesity on vertebral density and bone turnover in postmenopausal women

Ribot, C.; Trémollières, Florence; Pouillès, J. M.; Bonneu, Michel; Germain, François; Jp, Louvet

doi:10.1016/8756-3282(87)90062-7

Cited by 168 publications

(65 citation statements)

References 30 publications

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“…These results agree with those reported in other studies, but their significance is not fully understood (24). In other situations in which there is a reduction of osteocalcin levels, both protection (e.g., in obesity) (25,26) and impairment (e.g., in old age) (27)(28)(29) of bone mass have been observed. It is interesting to observe that, regarding the other biochemical parameter of bone formation, i.e., PICP, the serum levels of the three groups were similar.…”

Section: Discussionsupporting

confidence: 82%

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Cutrim¹,

Pereira²,

Paula³

et al. 2007

Braz J Med Biol Res

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We assessed the effect of chronic hyperglycemia on bone mineral density (BMD) and bone remodeling in patients with type 2 diabetes mellitus. We investigated 42 patients with type 2 diabetes under stable control for at least 1 year, 22 of them with good metabolic control (GMC: mean age = 48.8 ± 1.5 years, 11 females) and 20 with poor metabolic control (PMC: mean age = 50.2 ± 1.2 years, 8 females), and 24 normal control individuals (CG: mean age = 46.5 ± 1.1 years, 14 females). We determined BMD in the femoral neck and at the L2-L4 level (DEXA) and serum levels of glucose, total glycated hemoglobin (HbA 1 ), total and ionic calcium, phosphorus, alkaline phosphatase, follicle-stimulating hormone, intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25-OH-D), insulin-like growth factor I (IGFI), osteocalcin, procollagen type I C propeptide, as well as urinary levels of deoxypyridinoline and creatinine. HbA 1 levels were significantly higher in PMC patients (12.5 ± 0.6 vs 7.45 ± 0.2% for GMC and 6.3 ± 0.9% for CG; P < 0.05). There was no difference in 25-OH-D, iPTH or IGFI levels between the three groups. BMD values at L2-L4 (CG = 1.068 ± 0.02 vs GMC = 1.170 ± 0.03 vs PMC = 1.084 ± 0.02 g/cm 2 ) and in the femoral neck (CG = 0.898 ± 0.03 vs GMC = 0.929 ± 0.03 vs PMC = 0.914 ± 0.03 g/cm 2 ) were similar for all groups. PMC presented significantly lower osteocalcin levels than the other two groups, whereas no significant difference in urinary deoxypyridine was observed between groups. The present results demonstrate that hyperglycemia is not associated with increased bone resorption in type 2 diabetes mellitus and that BMD is not altered in type 2 diabetes mellitus.

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Section: Discussionsupporting

confidence: 82%

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Cutrim¹,

Pereira²,

Paula³

et al. 2007

Braz J Med Biol Res

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“…There are many reports indicating that osteoporosis and particularly hip fractures are less frequent in obese subjects (10)(11)(12)(13). Obese and overweight women have a greater bone mass after menopause than lean women of the same age (10,13). This protective effect appears to be related to both a high fat content and mechanical factors (13).…”

Section: Discussionmentioning

confidence: 99%

“…Obese and overweight women have a greater bone mass after menopause than lean women of the same age (10,13). This protective effect appears to be related to both a high fat content and mechanical factors (13). Some studies suggest that greater concentrations of estrogen, decreased sex hormone binding globulin and increased free sex steroids, insulin-like growth factor-I and hyperinsulinemia are responsible for greater bone mass in obese women (10,13).…”

Section: Discussionmentioning

confidence: 99%

“…These findings suggest that circulating plasma leptin does not have a direct influence on bone mass in postmenopausal women. There are many reports indicating that osteoporosis and particularly hip fractures are less frequent in obese subjects (10)(11)(12)(13). Obese and overweight women have a greater bone mass after menopause than lean women of the same age (10,13).…”

Section: Discussionmentioning

confidence: 99%

“…This has been attributed to the mechanical effects of their excessive weight on bone tissue. Obese postmenopausal women have a tendency to have increased bone mineral density compared with lean women (11)(12)(13). A recent in vitro study demonstrated that leptin acts on human marrow stromal cells to enhance differentiation to osteoblasts, suggesting a role of leptin in bone metabolism (14).…”

Section: Introductionmentioning

confidence: 99%

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Plasma leptin concentrations in postmenopausal women with osteoporosis

Odabaşı¹,

Özata

Turan³

et al. 2000

European Journal of Endocrinology

100

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Background: The obese are usually protected against osteoporosis and have increased bone mineral density and plasma leptin concentrations. A recent in vitro study demonstrated that leptin acts on human marrow stromal cells to enhance differentiation to osteoblasts, suggesting an influence of leptin on bone mass. However, little is known about the relationship between plasma leptin and bone mass in postmenopausal women with osteoporosis. Objective: To investigate plasma leptin concentrations in postmenopausal women with osteoporosis to improve the understanding of the role of leptin in determining bone mass. Methods: Fifty postmenopausal women with osteoporosis (ages 61.18 Ϯ 6.51 years; body mass index (BMI) 28.91 Ϯ 3.44 kg/m

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Perspectives: A biomechanical model of the pathogenesis of arthroses

Frost

1994

Anat. Rec.

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This model views the common, initiating cause of arthroses as excessive articular cartilage microdamage. If so, understanding it would become a central problem for understanding the pathogenesis of arthroses. The model proposes the microdamage can stem from: (1) Excessive total loads on normal joints; (2) underadaptations in a joint's size or shape that leave its momentarily loaded area too small for normal loads; (3) impaired microdamage repair in subchondral bone or articular cartilage; (4) abnormal composition or structure that makes a tissue develop excessive microdamage under normal loads. (5) (2)-(4) above could stem from changed set points or "lead times" for a joint's adaptations and maintenance, which in turn could stem from (6) genetic influences, some drugs, toxins, diseases, and "X," and (7) from combinations of the above. In the pathogenesis of arthroses this model assigns special importance to the stiffness of joint tissues (as distinguished from their strength), to the typical largest unit loads they carry as a result of a subject's usual physical activities, and to microdamage in those tissues.

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Obesity and postmenopausal bone loss: The influence of obesity on vertebral density and bone turnover in postmenopausal women

Cited by 168 publications

References 30 publications

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Plasma leptin concentrations in postmenopausal women with osteoporosis

Perspectives: A biomechanical model of the pathogenesis of arthroses

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