Abstract
Sirtuin1 (SIRT1) and sclerostin play important roles in adipose tissue and bone metabolism. We evaluated the circulating SIRT1 and sclerostin relationship with mass and quality of bone while considering the degree of adiposity. Sixty-six premenopausal women (16 underweight, 25 normal weight and 25 with obesity), aged <50 years, were enrolled. Plasma SIRT1, sclerostin and DXA body composition (total fat mass (FM), abdominal visceral adipose tissue, lean mass, trabecular bone score (TBS) and lumbar spine and femoral neck (FN) bone mineral density (BMD)) were assessed. The patients with obesity showed the lowest SIRT1 and TBS values and the highest sclerostin concentrations; BMD increased with FM and BMI and had an inverse association with SIRT1. Sclerostin was negatively correlated with SIRT1 (ρ = −0.37, p = 0.002). When spine BMD, FN BMD and TBS were standardized for BMI, a positive correlation with SIRT1 and a negative correlation with sclerostin were seen (p < 0.005). In the regression analysis, sclerostin was the best independent, negative predictor for BMD and TBS, while SIRT1 directly predicted TBS (p < 0.05). In conclusion, blood measurement of SIRT1 and sclerostin could represent a snapshot of the bone status that, taking into account the degree of adiposity, may reduce the interference of confounding factors in the interpretation of bone health parameters.
Highlights
Bone mass loss, as occurs in osteopenia and osteoporosis, is one of the most common metabolic bone disorders [1]
We found that circulating SIRT1 and sclerostin were linked by an inverse association across different fat mass degrees and that they had a consistent relationship with the bone mass
In line with these results, we found that the levels of sclerostin increased in parallel with fat mass (FM)%, abdominal visceral adipose tissue (VAT), trunk/legs FM and glycemia, and that plasma SIRT1 behaved in the opposite way
Summary
As occurs in osteopenia and osteoporosis, is one of the most common metabolic bone disorders [1]. Many factors have been associated with a higher risk of bone demineralization, including age, prolonged glucocorticoids treatment or estrogen deprivation. Obesity is associated with an increased risk of fracture in some reports, possibly due to the trabecular bone metabolic and microcirculatory derangements responsible for microarchitecture alteration [4–6]. In this regard, the trabecular bone score (TBS) has recently emerged as a useful clinical parameter of bone microarchitecture degradation and is found to be sensitive to glycometabolic alterations [7]. The pathophysiology underlying the link between bone and fat, as well as its possible means of evaluation, are still a matter of debate, and several molecules possibly involved were recently described
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