The incidence and prevalence of metabolic and musculoskeletal diseases are increasing. Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance, inflammation, advanced glycation end-product accumulation and increased oxidative stress. These characteristics can negatively affect various aspects of muscle health, including muscle mass, strength, quality and function through impairments in protein metabolism, vascular and mitochondrial dysfunction, and cell death. Sarcopenia is a term used to describe the agerelated loss in skeletal muscle mass and function and has been implicated as both a cause and consequence of T2DM. Sarcopenia may contribute to the development and progression of T2DM through altered glucose disposal due to low muscle mass, and also increased localized inflammation, which can arise through inter-and intramuscular adipose tissue accumulation. Lifestyle modifications are important for improving and maintaining mobility and metabolic health in individuals with T2DM and sarcopenia. However, evidence for the most effective and feasible exercise and dietary interventions in this population is lacking. In this review, we discuss the current literature highlighting the bidirectional relationship between T2DM and sarcopenia, highlight current research gaps and treatments, and provide recommendations for future research.

Ageing, obesity and the metabolic syndrome (MetS) may all contribute to poor muscle health (sarcopenia). This study aimed to determine the cross-sectional associations between MetS (International Diabetes Federation classification) and sarcopenia (revised European Working Group on Sarcopenia in Older People definition) in 84 overweight and obese older adults. Components of sarcopenia included muscle strength (hand grip and leg extension), physical performance (stair climb test and short physical performance battery (SPPB), including gait speed and repeated chair stands time), muscle mass (appendicular lean mass (ALM), dual-energy X-ray absorptiometry), muscle size (peripheral quantitative computed tomography-determined calf and forearm cross-sectional area (CSA)) and muscle quality (muscle density and strength normalised to lean mass). Waist circumference was associated with greater muscle size, but poorer leg extension strength, chair stands and stair climb time, gait speed, SPPB scores and muscle quality measures (all p < 0.05). MetS was positively associated with ALM and forearm muscle CSA, and negatively associated with muscle quality measures and chair stands time (all p < 0.05). MetS is associated with larger muscle size, yet poorer muscle quality in overweight and obese older adults. Assessments of muscle function and quality should be considered for obese older adults and those with MetS.

Summary Sarcopenia and obesity are common conditions in older adults that may have differing effects on falls and fracture risk. This systematic review and meta‐analysis aimed to determine whether older adults with sarcopenic obesity have increased risk of falls and fractures or lower bone mass compared with older adults with sarcopenia, obesity, or neither condition. Twenty‐six studies (n = 37,124) were included in the systematic review and 17 (n = 31,540) were included in the meta‐analysis. Older adults with sarcopenic obesity had lower femoral neck areal bone mineral density (aBMD) compared with those with obesity alone but had higher femoral neck aBMD compared with counterparts with sarcopenia alone (both P < 0.05). Older adults with sarcopenic obesity had higher nonvertebral fracture rates (incidence rate ratio: 1.88; 95% confidence intervals: 1.09, 3.23; based on two studies), compared with those with sarcopenia alone, and also had higher falls risk compared with controls (risk ratio: 1.30; 95% confidence intervals: 1.10, 1.54) and obesity alone (risk ratio: 1.17; 95% confidence intervals: 1.01, 1.36). In conclusion, this systematic review and meta‐analysis has demonstrated that older adults with sarcopenic obesity are at increased risk of adverse musculoskeletal outcomes compared with individuals with obesity, sarcopenia, or neither condition. These data support the need for developing interventions to improve bone health and physical function in this population.

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Background Vitamin D supplementation is proposed as a potentially effective nutritional intervention to mitigate the risk of sarcopenia. The aim of this systematic review and meta-analysis was to investigate the impact of vitamin D supplementation monotherapy on indices of sarcopenia in community-dwelling older adults. Methods A comprehensive search of the literature was conducted in PubMed, Web of Science, Scopus, and Cochrane Library. Eligible randomized controlled trials (RCTs) compared the effect of vitamin D supplementation (as monotherapy) with placebo on indices of sarcopenia in older (>50 years) adults. Using the random effects inverse-variance model, we calculated the mean difference (MD) in handgrip strength (HGS), short physical performance battery (SPPB), timed up and go (TUG), and appendicular lean mass (ALM) between groups. We also calculated the standardized mean difference (SMD) in general muscle strength and general physical performance (composite plot of all muscle strength and physical performance outcomes, respectively) between groups. Results Ten RCTs were included in the meta-analysis. A significant decrease in SPPB scores was observed with vitamin D supplementation compared with placebo (MD: À0.23; 95% CI À0.40 to À0.06; I 2 = 0%; P = 0.007). Vitamin D supplementation conferred no effect on HGS (MD: À0.07 kg; 95% CI À0.70 to 0.55; I 2 = 51%, P = 0.82), TUG (MD: 0.07 s; 95% CI À0.08 to 0.22; I 2 = 0%, P = 0.35), ALM (MD: 0.06 kg/m 2 ; 95% CI: À0.32 to 0.44; I 2 = 73%, P = 0.77), general muscle strength (SMD: À0.01; 95% CI À0.17 to 0.15; I 2 = 42%, P = 0.90), or general physical performance (SMD: À0.02; 95% CI À0.23 to 0.18; I 2 = 71%, P = 0.83). Conclusions Vitamin D supplementation did not improve any sarcopenia indices in community-dwelling older adults and may compromise some aspects of physical performance. Future studies are warranted to investigate the impact of vitamin D supplementation on individual indices of SPPB, including mobility and balance, in older adults.

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Background Weight-loss-induced fat loss improves cardiometabolic health in individuals with overweight and obesity; however, weight loss can also result in bone loss and increased fracture risk. Weight-loss-induced bone loss may be attenuated with exercise. Our aim was to compare changes in bone mineral density (BMD) in adults with overweight and obesity who undertook diet-induced weight loss alone or in combination with exercise. Methods We included randomized controlled trials (RCTs) in adults with overweight or obesity (aged ≥18 years; body mass index ≥25 kg/m 2 ) that prescribed diet-induced weight loss alone or in combination with supervised exercise, and measured any bone structural parameters. Risk of bias was assessed using the Cochrane Risk of Bias tool. Random-effects meta-analyses determined mean changes and net mean differences (95% confidence intervals (95%CIs)) in the percentage of areal BMD (aBMD) change between groups. Results We included 9 RCTs. Diet-induced weight loss led to significant losses in femoral neck aBMD (mean change: −1.73% (95%CI: −2.39% to −1.07%), p < 0.001) and total hip aBMD (−2.19% (95%CI: −3.84% to −0.54%), p = 0.009). Femoral neck aBMD losses were significantly greater in the diet-induced weight loss group compared to the exercise plus diet-induced weight loss group (net difference: −0.88% (95%CI: −1.73% to −0.03%)); however, there were no differences in aBMD changes at any other skeletal site: total hip (−1.96% (95%CI: −4.59% to 0.68%)) and lumbar spine (−0.48% (95%CI: −1.81% to 0.86%)). aBMD changes did not differ significantly according to exercise modality (resistance exercise, aerobic exercise, or a combination of the two) during diet-induced weight loss. Conclusion Diet-induced weight loss led to greater femoral neck bone loss compared to diet-induced weight loss plus exercise. Bone loss at the total hip and lumbar spine was not attenuated by exercise during diet-induced weight loss. The lack of consistent skeletal benefits may be due to the insufficient duration and/or training intensities of most exercise interventions. Additional RCTs with appropriate, targeted exercise interventions should be conducted.