Background: Obesity is a pathological condition that has reached epidemic proportions; hence, it is necessary to find novel strategies aimed at fighting this disease. The present study was designed to evaluate the effect of a flavonoid-rich extract of orange (Citrus sinensis) juice (OJe) in diet-induced obese zebrafish. Methods: Adult zebrafish were divided into four diet groups: (i) normally fed (NF); (ii) overfed (OF); (iii) NF supplemented with OJe (5 mL/L in fish water; NF + OJe); and (iv) OF supplemented with OJe (OF + OJe). Each week, body weight (BW) and body mass index (BMI) were measured, and, at the end of the fifth week, euthanized zebrafish were processed for both microscopic evaluations and qPCR analyses. Results: In OF zebrafish, OJe significantly decreased both BW and BMI values and lowered the visceral adipose tissue, while it had little effect in the NF group. Moreover, it significantly reduced adipocyte cell size in both NF and OF groups in both visceral and subcutaneous adipose tissues, as well as their number in OF fish. Finally, OJe modulated some obesity-related genes, such as leptin A, ghrelin, orexin, pro-opiomelanocortin (POMC), and neuropeptide Y (NPY), in both gut and brain. Conclusion: This study adds new insights into the anti-obesity properties of orange juice and its flavonoids, suggesting their role as weight management agents through a lipolytic action linked to a restoration of metabolism-regulating gene expression.

Bisphosphonates (BPs) are inhibitors of osteoclast‐mediated bone resorption used for the treatment of multiple myeloma (MM) patients with osteolytic lesions. Bisphosphonate‐induced osteonecrosis of the jaw (BONJ) is an infrequent drug‐caused adverse event of these agents. Long noncoding RNAs (lncRNAs) are a set of more than 200 base pairs, noncoding RNA molecules, which are critical posttranscriptional regulators of gene expression. Our study was aimed at evaluating 17 lncRNAs, whose targets were previously validated as key elements in MM, bone metabolism, and angiogenesis in MM subjects without BONJ (MM group), in MM subjects with BONJ (BONJ group), and a group of healthy controls (CTRL group). Our results demonstrated a different lncRNA profile in BONJ patients compared to MM patients and controls. Two lncRNAs (DANCR and MALAT1) were both downregulated compared to controls and MM, twelve (HOTAIR, MEG3, TP73‐AS1, HOTTIP, HIF1A‐AS2, MANTIS, CTD‐2201E18, CTD1‐2003C8, R‐471B22, RP1‐43E13, RP11‐553L6.5, and RP1‐286D6) were overexpressed in MM with BONJ, and one (H19) was upregulated compared with only MM. Two lncRNAs (JHDMD1 and MTMR9LP) had higher expression, but these differences were not statistically significant. The examined lncRNAs target several genes and metabolic pathways. An altered lncRNA signature could contribute to the onset of BONJ or have a protective action. Targeting these lncRNAs could offer a possibility for the prevention or therapy of BONJ.