Complex interplay among adiposity, insulin resistance and bone health

Ma, Chunxiao; Tonks, Katherine T.; Samocha-Bonet, Dorit; Greenfield, Jerry R.

doi:10.1111/cob.12240

Cited by 27 publications

(23 citation statements)

References 118 publications

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“…Patho-physiologically, T2DM is associated with insulin resistance. Therefore, cells from patients living with diabetes mellitus are less likely to accumulate lipids [159]. Increased bone marrow adiposity is known to correlate with altered levels of growth hormones, increased visceral adiposity, increased circulating lipids, and hypoleptinemia [28].…”

Section: Effect Of Diabetes On Progenitor Cellsmentioning

confidence: 99%

Impact of Diabetes Mellitus on Bone Health

Murray

Coleman

2019

IJMS

150

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Long-term exposure to a diabetic environment leads to changes in bone metabolism and impaired bone micro-architecture through a variety of mechanisms on molecular and structural levels. These changes predispose the bone to an increased fracture risk and impaired osseus healing. In a clinical practice, adequate control of diabetes mellitus is essential for preventing detrimental effects on bone health. Alternative fracture risk assessment tools may be needed to accurately determine fracture risk in patients living with diabetes mellitus. Currently, there is no conclusive model explaining the mechanism of action of diabetes mellitus on bone health, particularly in view of progenitor cells. In this review, the best available literature on the impact of diabetes mellitus on bone health in vitro and in vivo is summarised with an emphasis on future translational research opportunities in this field.

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Section: Effect Of Diabetes On Progenitor Cellsmentioning

confidence: 99%

Impact of Diabetes Mellitus on Bone Health

Murray

Coleman

2019

IJMS

150

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“…22 Obesity is associated with adverse changes in bone health via several mechanisms, including alteration of bone-regulating hormones, increased oxidative stress and inflammation, and altered bone cell metabolism. 23 Obesity may negatively affect bone quality. A greater risk of bone fracture for a given BMD value has been observed in the obese population.…”

Section: Introductionmentioning

confidence: 99%

Association of Fat Body Mass With Vertebral Fractures in Postmenopausal Women With Early Breast Cancer Undergoing Adjuvant Aromatase Inhibitor Therapy

et al. 2019

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Key PointsQuestionIs fat body mass associated with the prevalence of vertebral fracture in patients with breast cancer undergoing aromatase inhibitor therapy?FindingsThis cross-sectional study of 556 postmenopausal women with early-stage breast cancer treated with aromatase inhibitors found that high fat body mass was associated with a numerically but not significantly lower proportion of vertebral fractures in aromatase inhibitor–naive women and a significantly higher proportion of vertebral fractures in aromatase inhibitor–treated women. This opposite trend in fracture prevalence was confirmed after propensity-score matching.MeaningFat body mass may be a factor associated with vertebral fractures in postmenopausal women with breast cancer receiving aromatase inhibitors.

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“…The overexpression of c-Fos in mice BMMs also induces the formation of osteoclasts via activation of NF-κB, JNK, p38 and ERK (Kim et al, 2009). Moreover, IL-1 causes bone loss by promoting osteoclast precursor fusion and enhancing the differentiation of osteoclasts into mature osteoclasts (Ma et al, 2018).…”

Section: Phosphorylation Of Ampk Inhibits Osteoclast Differentiation mentioning

confidence: 99%

AMP‐activated protein kinase (AMPK) regulates autophagy, inflammation and immunity and contributes to osteoclast differentiation and functionabs

Tong

Ganta

Liu

2020

Biology of the Cell

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Osteoclasts are multinucleated giant cells, responsible for bone resorption. Osteoclast differentiation and function requires a series of cytokines to remove the old bone, which coordinates with the induction of bone remodelling by osteoblast‐mediated bone formation. Studies have demonstrated that AMP‐activated protein kinase (AMPK) play a negative regulatory role in osteoclast differentiation and function. Research involving AMPK, a nutrient and energy sensor, has primarily focused on osteoclast differentiation and function; thus, its role in autophagy, inflammation and immunity remains poorly understood. Autophagy is a conservative homoeostatic mechanism of eukaryotic cells, and response to osteoclast differentiation and function; however, how it interacts with inflammation remains unclear. Additionally, based on the regulatory function of different AMPK subunits for osteoclast differentiation and function, its activation is regulated by upstream factors to perform bone metabolism. This review summarises the critical role of AMPK‐mediated autophagy, inflammation and immunity by upstream and downstream signalling during receptor activator of nuclear factor kappa‐B ligand‐induced osteoclast differentiation and function. This pathway may provide therapeutic targets for bone‐related diseases, as well as function as a biomarker for bone homoeostasis.

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Complex interplay among adiposity, insulin resistance and bone health

Cited by 27 publications

References 118 publications

Impact of Diabetes Mellitus on Bone Health

Impact of Diabetes Mellitus on Bone Health

Association of Fat Body Mass With Vertebral Fractures in Postmenopausal Women With Early Breast Cancer Undergoing Adjuvant Aromatase Inhibitor Therapy

AMP‐activated protein kinase (AMPK) regulates autophagy, inflammation and immunity and contributes to osteoclast differentiation and functionabs

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