About Prof. Liu Jianmin
Prof. Liu Jianmin is a senior endocrinologist at Ruijin Hospital, Shanghai Jiao Tong University School of Medicine — one of China's foremost centres for endocrinology, metabolic disease, and neuroendocrinology. He specialises in the diagnosis and management of pituitary tumours, thyroid disorders, and complex diabetes cases, and is a nationally recognised leader in neuroendocrinology and metabolic disease. His research programme has made foundational contributions to understanding the relationship between diabetes and skeletal health — demonstrating that diabetic patients face significantly elevated fracture risk even when bone mineral density appears normal, and that bone-derived hormones such as osteocalcin and lipocalin-2 play active roles in glucose metabolism and insulin sensitivity. His clinical philosophy holds that diabetes is a systemic disease, and that its management must be equally systemic: glycaemic control, bone health, neuropathy, cardiovascular risk, and renal function are not separate problems to be addressed by separate specialists — they are interconnected dimensions of a single patient's metabolic reality, and they must be managed together.
Case Overview
Mr. Fang (pseudonym), a 62-year-old man with a 14-year history of type 2 diabetes and established peripheral neuropathy, presented following a low-energy fall that resulted in a fragility fracture of the left distal radius. His HbA1c was 8.4% and he had been on a stable oral hypoglycaemic regimen for several years. Dual-energy X-ray absorptiometry (DXA) showed bone mineral density in the osteopenic range — not severely reduced, but below the threshold expected for his age. High-resolution peripheral quantitative CT (HR-pQCT) revealed significantly impaired trabecular microstructure and cortical porosity disproportionate to his DXA result, consistent with the pattern of diabetic bone disease: preserved or near-normal BMD masking substantial deterioration in bone quality. Prof. Liu Jianmin's multidisciplinary assessment — endocrinology, orthopaedics, and neurology — identified three interconnected drivers of fracture risk: suboptimal glycaemic control accelerating bone microstructural deterioration; peripheral neuropathy increasing fall risk; and his existing oral hypoglycaemic regimen including a thiazolidinedione, a drug class associated with reduced bone formation. A personalised integrated management plan was formulated: glycaemic regimen restructuring to eliminate bone-adverse agents and optimise HbA1c; bone-protective pharmacotherapy; neuropathy management and fall prevention; and structured follow-up with serial bone imaging. At twelve-month review, HbA1c had improved to 7.0%; bone turnover markers showed a favourable response to treatment; and Mr. Fang reported a significant improvement in confidence and physical activity. He reflected: "I did not realise that my diabetes was affecting my bones. Prof. Liu's team explained everything clearly and gave me a plan that addressed all of it together. I feel much more in control of my health now."
Diagnostic Workup
DXA of the lumbar spine and bilateral hips quantified bone mineral density and T-scores, establishing the osteopenic baseline and providing a reference for treatment response monitoring. HR-pQCT of the distal radius and tibia characterised trabecular microstructure, cortical thickness, and cortical porosity — revealing bone quality impairment substantially greater than the DXA result suggested, consistent with the diabetic bone phenotype. Bone turnover markers — osteocalcin (bone formation) and serum CTX (bone resorption) — were measured at baseline; low osteocalcin was noted, consistent with suppressed bone formation in the context of chronic hyperglycaemia. Comprehensive metabolic assessment included HbA1c, fasting glucose, renal function, vitamin D, calcium, phosphate, and parathyroid hormone. Peripheral neuropathy was assessed with nerve conduction studies and the Michigan Neuropathy Screening Instrument. Medication review identified thiazolidinedione use as a modifiable bone-adverse factor. Multidisciplinary review confirmed the integrated management strategy.
Prof. Liu's pre-treatment assessment: The DXA result alone would not have told us the full story. In diabetic patients, bone mineral density frequently underestimates fracture risk because the microstructural damage — the trabecular deterioration and cortical porosity — is not captured by DXA. The HR-pQCT result explains why this patient fractured at a BMD level that would not ordinarily predict fracture. The neuropathy is the other critical factor: it increases fall frequency, and in a patient whose bone quality is already compromised, falls are the proximate cause of fractures. We need to address both the bone and the fall risk simultaneously — and we need to restructure the glycaemic regimen to remove the agent that is actively suppressing bone formation.
Treatment Strategy and Course
Diagnosis: Type 2 Diabetes with Peripheral Neuropathy, Osteopenia with Significantly Impaired Bone Microstructure (Diabetic Bone Disease), and Left Distal Radius Fragility Fracture in a 62-year-old patient.
Treatment principle: integrated personalised management addressing glycaemic optimisation, elimination of bone-adverse medications, bone-protective pharmacotherapy, neuropathy management, and fall prevention — coordinated as a unified strategy rather than sequential specialist referrals.
- Glycaemic regimen restructuring: Thiazolidinedione discontinued; regimen transitioned to an SGLT2 inhibitor and GLP-1 receptor agonist combination — both with neutral or favourable bone profiles and established cardiovascular and renal benefits; target HbA1c set at 7.0% or below
- Bone-protective pharmacotherapy: Vitamin D and calcium supplementation initiated to correct insufficiency; antiresorptive therapy commenced following assessment of renal function and dental status; treatment duration and monitoring schedule established per the Chinese Expert Consensus on Fracture Risk Management in Diabetic Patients (co-authored by Prof. Liu's team)
- Neuropathy management and fall prevention: Neurological review confirmed peripheral neuropathy severity; pharmacological neuropathy management optimised; physiotherapy referral for balance training and fall prevention programme; home environment assessment recommended
- Fracture rehabilitation: Orthopaedic management of the left distal radius fracture; cast immobilisation followed by supervised hand therapy; full functional recovery of the left wrist achieved by week ten
- Twelve-month follow-up: HbA1c 7.0% (from 8.4% at presentation); bone turnover markers: osteocalcin normalised, CTX within target range for antiresorptive therapy; repeat DXA: lumbar spine BMD increased by 3.2%; no further fractures; neuropathy symptoms stable; patient reported significantly improved confidence in physical activity and daily function
Prof. Liu's clinical reflection: The outcome at twelve months reflects what integrated management can achieve when the connections between diabetes and bone health are recognised and acted upon from the outset. The glycaemic improvement, the bone turnover marker response, and the absence of further fractures are not independent results — they are the product of a strategy that addressed the metabolic, pharmacological, and functional dimensions of this patient's risk simultaneously. The thiazolidinedione switch alone removed a significant suppressant of bone formation. The fall prevention programme addressed the proximate cause of fracture. The antiresorptive therapy addressed the structural deficit. Together, they changed the trajectory.
Expert Commentary — Prof. Liu Jianmin
1. The Diabetic Bone Phenotype: Why BMD Underestimates Fracture Risk in Diabetes
The relationship between diabetes and fracture risk is paradoxical and clinically underappreciated. In type 1 diabetes, bone mineral density is reduced and fracture risk is elevated — a straightforward relationship. In type 2 diabetes, the picture is more complex: BMD is frequently normal or even elevated relative to age-matched controls, yet fracture risk is significantly increased — by approximately 40% for hip fracture and substantially more for other sites. This paradox is explained by the diabetic bone phenotype: chronic hyperglycaemia and advanced glycation end-products (AGEs) accumulate in bone collagen, impairing its mechanical properties and reducing bone toughness without necessarily reducing bone mass. Trabecular microstructure deteriorates — as demonstrated by HR-pQCT — and cortical porosity increases, reducing bone strength in ways that DXA cannot detect. The clinical implication is that standard fracture risk assessment tools, which rely heavily on BMD, systematically underestimate fracture risk in diabetic patients. Prof. Liu's team has contributed to the evidence base establishing this phenotype and to the development of clinical consensus guidance incorporating diabetes-specific fracture risk assessment.
2. Bone-Derived Hormones and Glucose Metabolism: The Skeleton as an Endocrine Organ
Research from Prof. Liu Jianmin's group and collaborating laboratories has contributed to a fundamental reconceptualisation of the skeleton — from a passive structural organ to an active endocrine organ with bidirectional metabolic signalling. Osteocalcin, a protein secreted by osteoblasts, has been shown in experimental models to lower blood glucose in diabetic mice and to enhance insulin sensitivity — establishing a direct link between bone formation activity and glucose homeostasis. Lipocalin-2, another osteoblast-derived factor, has been shown to suppress appetite and improve insulin resistance. Conversely, bone resorption markers such as CTX have been identified as potential predictors of diabetes onset, suggesting that bone turnover dynamics reflect and influence metabolic risk. These findings have reframed the clinical relationship between diabetes and bone health: it is not simply that diabetes damages bone, but that bone and metabolic function are in continuous bidirectional dialogue. The clinical translation of this research — using osteocalcin and CTX as metabolic biomarkers, and recognising that bone-protective therapy may have metabolic as well as skeletal benefits — is an active area of investigation.
3. Medication Effects on Bone Health in Diabetes: A Framework for Prescribing Decisions
The choice of glucose-lowering therapy in patients with diabetes and elevated fracture risk requires explicit consideration of each agent's skeletal effects — a dimension of prescribing that has historically received insufficient attention. Thiazolidinediones (TZDs) are the most clearly bone-adverse class: they activate PPAR-γ in bone marrow stromal cells, diverting differentiation away from osteoblasts toward adipocytes, suppressing bone formation, and increasing fracture risk — particularly at peripheral sites in women. SGLT2 inhibitors have a more nuanced profile: some studies suggest modest effects on BMD, but their cardiovascular and renal benefits frequently outweigh skeletal concerns in appropriately selected patients, and they do not carry the clear bone-adverse signal of TZDs. GLP-1 receptor agonists appear to have a neutral or potentially favourable bone profile. Insulin, used appropriately, does not adversely affect bone. The practical framework for prescribing in patients with diabetes and fracture risk is to avoid TZDs where alternatives exist, to prefer agents with neutral or favourable bone profiles, and to integrate bone health monitoring — DXA, bone turnover markers, and fracture risk assessment — into the routine management of patients with longstanding diabetes, neuropathy, or prior fragility fracture.
How CMCS Shanghai Coordinated This Case
CMCS Shanghai supported Mr. Fang and his family throughout the diagnostic, treatment, and follow-up pathway at Ruijin Hospital, Shanghai Jiao Tong University, including: priority consultation coordination with Prof. Liu Jianmin's endocrinology team; bilingual interpretation across all endocrinology, orthopaedic, and neurology consultations and follow-up appointments; bilingual explanation of the diabetic bone phenotype, the fracture risk assessment findings, and the integrated management strategy; coordination of DXA, HR-pQCT, bone turnover markers, nerve conduction studies, and comprehensive metabolic assessment with bilingual results communication; bilingual medication counselling for the glycaemic regimen restructuring and bone-protective therapy; coordination of physiotherapy and fall prevention programme referral; orthopaedic fracture management coordination including cast care and hand therapy scheduling; and twelve-month follow-up coordination including repeat DXA, bone turnover marker monitoring, and HbA1c surveillance.
For international patients and expatriates in China living with diabetes — particularly those with longstanding disease, peripheral neuropathy, or concerns about bone health and fracture risk — Prof. Liu Jianmin's team at Ruijin Hospital offers access to one of China's most experienced and research-active endocrinology and metabolic bone disease programmes. CMCS ensures that expertise is accessible — in the patient's language, with every step coordinated and communicated clearly.
This case report is de-identified and published for educational purposes. All clinical details have been anonymized in accordance with patient privacy standards. CMCS Shanghai is a medical concierge service and does not provide direct medical care.
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