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Bone Metabolism and Diseases / GDF15 and Related Biomarkers · Journal article
International Journal of Molecular Medicine · August 17, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review proposing that abnormal glucose metabolism is a key pathogenic mechanism in osteoporosis and that insulin signaling may represent a therapeutic target. The work integrates mechanistic observations about aerobic and anaerobic metabolism in bone cells and describes how metabolic dysfunction occurs in postmenopausal women, type 2 diabetes, and obesity, but does not present clinical trial evidence or test this hypothesis empirically.
Journal article. Postmenopausal women, patients with type 2 diabetes mellitus, and individuals with obesity identified as high-risk populations for osteoporosis; no empirical cohort described..
Mesenchymal stem cells rely predominantly on glycolysis during commitment toward pre-osteoblasts, while maturation into functional osteoblasts depends more on oxidative phosphorylation. Osteoclast fusion and differentiation require robust mitochondrial oxidation. High-risk populations for osteoporosis include postmenopausal women, patients with type 2 diabetes mellitus, and individuals with obesity.
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This work frames glucose metabolism dysfunction as a potential therapeutic avenue in osteoporosis but does not provide evidence sufficient to guide clinical practice. Clinicians should recognize this as a mechanistic hypothesis requiring clinical validation before therapeutic implementation.
This is a narrative review synthesizing mechanistic evidence and pathophysiological theory about glucose metabolism in osteoporosis, proposing insulin signaling as a therapeutic target without reporting clinical trial data or direct evidence of efficacy.
This work frames glucose metabolism dysfunction as a potential therapeutic avenue in osteoporosis but does not provide evidence sufficient to guide clinical practice. Clinicians should recognize this as a mechanistic hypothesis requiring clinical validation before therapeutic implementation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Osteoporosis is a systemic skeletal disease characterized by progressive bone loss and an increased risk of fracture, and it represents a major public health challenge worldwide.Osteoporosis has multiple pathogenic determinants, including age, endocrine disorders and medication.Current therapeutic approaches primarily aim to promote osteogenesis directly or inhibit osteoclast activity; however, these strategies may limit therapeutic efficacy and increase the risk of adverse effects.The present review provided an integrated perspective on the pathogenesis of osteoporosis from the standpoint of glucose metabolism.Glucose oxidation generates ATP and metabolic intermediates that are key to bone homeostasis.During early differentiation, mesenchymal stem cells rely predominantly on glycolysis during commitment toward pre-osteoblasts, whereas maturation into functional osteoblasts depends more notably on oxidative phosphorylation.The fusion and differentiation of osteoclasts require robust mitochondrial oxidation.Lactate derived from anaerobic metabolism has a dual role in bone metabolism.High-risk populations for osteoporosis include postmenopausal women, patients with type 2 diabetes mellitus and individuals with obesity.Estrogen exerts anti-inflammatory and antioxidant effects through receptor activation.Excessive production of advanced glycation end-products disrupts the bone matrix, whereas hyperlipidemia promotes inflammatory factor-induced bone resorption.These pathological changes disrupt the insulin receptor substrate/PI3K/AKT signaling pathway, compromise glucose transporter-mediated cellular glucose uptake and thus, contribute to relative insulin resistance and insufficiency compared with physiological states.In conclusion, the present review demonstrated that abnormal glucose metabolism is a key pathogenic mechanism in osteoporosis and that targeting insulin signaling may represent a fundamental strategy for correcting glucose metabolic abnormalities across diverse etiologies.Contents 1. Introduction 2. Aerobic oxidation in osteogenesis and osteoclastogenesis 3. Anaerobic oxidation in osteogenesis and osteoclastogenesis 4. Metabolites and key regulatory enzymes of the PPP in bone metabolism 5. GLUTs in osteoblasts and osteoclasts 6. Glucose metabolism in muscle-bone crosstalk 7. Glucose metabolism in postmenopausal osteoporosis 8. Glucose metabolism in diabetic osteoporosis 9. Glucose metabolism in obesity-associated osteoporosis 10.Clinical evidence of therapeutic targets in high-risk populations for osteoporosis 11.
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