Accumulating evidence has shown that hydrogen sulfide (H₂S) acts as a signaling regulator in plants. Here we show that H₂S delays the postharvest senescence of broccoli in a dose-dependent manner. H₂S maintains higher levels of metabolites, such as carotenoids, anthocyanin, and ascorbate, and reduces the accumulation of malondialdehyde, H₂O₂, and the superoxide anion. Further investigations showed that H₂S sustained higher activities of guaiacol peroxidase, ascorbate peroxidase, catalase, and glutathione reductase and lower activities of lipoxygenase, polyphenol oxidase, phenylalanine ammonia lyase, and protease than those of water control. Moreover, the expression of the chlorophyll degradation related genes BoSGR, BoCLH2, BoPaO, BoRCCR, as well as cysteine protease BoCP1 and lipoxygenase gene BoLOX1, was down-regulated in postharvest broccoli treated with H₂S. The functions of H₂S on the senescence of other vegetables and fruits suggest its universal role acting as a senescence regulator.

KD is a relatively safe dietary therapy. However, because the KD can cause various AEs, it should be implemented under careful medical supervision. Continuous follow-up is needed to address the long-term impact of the diet on the overall health of children.

Obesity, overweight and autism spectrum disorder (ASD) remain serious public health problems. Although lots of studies have recently explored the association among obesity, overweight and ASD, the findings are inconsistent. Thus, we conducted a meta-analysis of epidemiological studies to examine the association among obesity, overweight and ASD. PubMed, Embase, and the Cochrane Library were used for literature searches to identify eligible studies published in English before November 15, 2016. Relevant studies estimating the association among obesity, overweight and ASD were included. Fifteen studies encompassing 49,937,078 participants and 1,045,538 individuals with ASD were included in this study. A random effects model was chosen to synthesize the effect sizes of individual studies. The prevalence of obesity was significantly higher in individuals with ASD than in controls (OR = 1.84, 95% confidence interval [CI]: 1.37–2.48, P < 0.001). However, the prevalence of overweight in individuals with ASD was not significantly different from that in controls (OR = 1.07, 95% CI: 0.83–1.38, P = 0.62). Both sensitivity analysis and publication bias testing revealed that the findings were robust. The meta-analysis showed a significant association between obesity and ASD. However, no significant association was identified between overweight and ASD.

Background Ctns−/− mice, a mouse model of infantile nephropathic cystinosis, exhibit hypermetabolism with adipose tissue browning and profound muscle wasting. Ctns−/− mice are 25(OH)D3 and 1,25(OH)2D3 insufficient. We investigated whether vitamin D repletion could ameliorate adipose tissue browning and muscle wasting in Ctns−/− mice. Methods Twelve‐month‐old Ctns−/− mice and wild‐type controls were treated with 25(OH)D3 and 1,25(OH)2D3 (75 μg/kg/day and 60 ng/kg/day, respectively) or an ethylene glycol vehicle for 6 weeks. Serum chemistry and parameters of energy homeostasis were measured. We quantitated total fat mass and studied expression of molecules regulating adipose tissue browning, energy metabolism, and inflammation. We measured lean mass content, skeletal muscle fibre size, in vivo muscle function (grip strength and rotarod activity), and expression of molecules regulating muscle metabolism. We also analysed the transcriptome of skeletal muscle in Ctns−/− mice using RNAseq. Results Supplementation of 25(OH)D3 and 1,25(OH)2D3 normalized serum concentration of 25(OH)D3 and 1,25(OH)2D3 in Ctns−/− mice, respectively. Repletion of vitamin D partially or fully normalized food intake, weight gain, gain of fat, and lean mass, improved energy homeostasis, and attenuated perturbations of uncoupling proteins and adenosine triphosphate content in adipose tissue and muscle in Ctns−/− mice. Vitamin D repletion attenuated elevated expression of beige adipose cell biomarkers (UCP‐1, CD137, Tmem26, and Tbx1) as well as aberrant expression of molecules implicated in adipose tissue browning (Cox2, Pgf2α, and NF‐κB pathway) in inguinal white adipose tissue in Ctns−/− mice. Vitamin D repletion normalized skeletal muscle fibre size and improved in vivo muscle function in Ctns−/− mice. This was accompanied by correcting the increased muscle catabolic signalling (increased protein contents of IL‐1β, IL‐6, and TNF‐α as well as an increased gene expression of Murf‐2, atrogin‐1, and myostatin) and promoting the decreased muscle regeneration and myogenesis process (decreased gene expression of Igf1, Pax7, and MyoD) in skeletal muscles of Ctns−/− mice. Muscle RNAseq analysis revealed aberrant gene expression profiles associated with reduced muscle and neuron regeneration, increased energy metabolism, and fibrosis in Ctns−/− mice. Importantly, repletion of 25(OH)D3 and 1,25(OH)2D3 normalized the top 20 differentially expressed genes in Ctns−/− mice. Conclusions We report the novel findings that correction of 25(OH)D3 and 1,25(OH)2D3 insufficiency reverses cachexia and may improve quality of life by restoring muscle function in an animal model of infantile nephropathic cystinosis. Mechanistically, vitamin D repletion attenuates adipose tissue browning and muscle wasting in Ctns−/− mice via multiple cellular and molecular mechanisms.