Bone health is the result of a tightly regulated balance between bone modeling and bone remodeling, and alterations of these processes have been observed in several diseases both in adult and pediatric populations. The imbalance in bone remodeling can ultimately lead to osteoporosis, which is most often associated with aging, but contributing factors can already act during the developmental age, when over a third of bone mass is accumulated. The maintenance of an adequate bone mass is influenced by genetic and environmental factors, such as physical activity and diet, and particularly by an adequate intake of calcium and vitamin D. In addition, it has been claimed that the integration of specific nutraceuticals such as resveratrol, anthocyanins, isoflavones, lycopene, curcumin, lutein, and β-carotene and the intake of bioactive compounds from the diet such as honey, tea, dried plums, blueberry, and olive oil can be efficient strategies for bone loss prevention. Nutraceuticals and functional foods are largely used to provide medical or health benefits, but there is an urge to determine which products have adequate clinical evidence and a strong safety profile. The aim of this review is to explore the scientific and clinical evidence of the positive role of nutraceuticals and functional food in bone health, focusing both on molecular mechanisms and on real-world studies.

Diabetic cardiomyopathy (DCM) represents one of the typical complications associated with diabetes. It has been described as anomalies in heart function and structure, with consequent high morbidity and mortality. DCM development can be described by two stages; the first is characterized by left ventricular hypertrophy and diastolic dysfunction, and the second by heart failure (HF) with systolic dysfunction. The proposed mechanisms involve cardiac inflammation, advanced glycation end products (AGEs) and angiotensin II. Furthermore, different studies have focused their attention on cardiomyocyte death through the different mechanisms of programmed cell death, such as apoptosis, autophagy, necrosis, pyroptosis and ferroptosis. Exosome release, adipose epicardial tissue and aquaporins affect DCM development. This review will focus on the description of the mechanisms involved in DCM progression and development.

Bone is a dynamic specialized connective tissue that undergoes continuous remodeling to preserve its health. Bone health is influenced throughout life by a combination of genetic, hormonal, and environmental factors, as well as physical activity and diet. This study aims to evaluate the effects of diets with different fat content on the femurs of mice fed for 16 or 20 weeks on a normal diet (ND16w and ND20w) or a Western diet (WD16w and WD20w) and for 20 weeks with their combinations on a ketogenic diet (KD) (WD + ND20w, ND + KD20w, and WD + KD20w). Micro-CT analysis on femoral cancellous bone revealed a non-significant trend toward decreased bone volume fraction (BV/TV) and trabecular thickness in mice fed a combined WD + KD20w compared to WD20w. Cortical bone thickness was significantly lower in mice fed WD16w and WD20w compared to those fed ND16w and ND20w (p = 0.049 and p = 0.039, respectively), in mice fed WD20w Ct.Th increased compared to WD + ND20w (p = 0.024) and a strong decrease is evident when comparing WD + ND20w to WD + KD20w (p < 0.0004). Consistently, histological analysis revealed that the number of osteoclasts per bone perimeter on cancellous bone increases compared with ND20w with ND + KD20w (p = 0.007) and WD + ND20w with ND + KD20w (p = 0.0006). In addition, a decrease in osteoblasts was observed (p < 0.041) in cortical bone, comparing ND20w with ND + KD20w; this suggests that the KD may have differential effects depending on the baseline condition. Osteocyte numbers did not significantly change when comparing the different treatments. Masson staining supports micro-CT results on both cortical and cancellous bone. In conclusion, transition from a high-fat diet to a normal diet may partially restore cortical bone health, whereas transition to a ketogenic diet exerts a trend toward additional detrimental effects on trabecular bone.