Formation of furan in baby food products: Identification and technical challenges.

Furan is generally produced during thermal processing of various foods including baked, fried, and roasted food items such as cereal products, coffee, canned, and jarred prepared foods as well as in baby foods. Furan is a toxic and carcinogenic compound to humans and may be a vital hazard to infants and babies. Furan could be formed in foods through thermal degradation of carbohydrates, dissociation of amino acids, and oxidation of polyunsaturated fatty acids. The detection of furan in food products is difficult due to its high volatility and low molecular weight. Headspace solid-phase microextraction coupled with gas chromatography/mass spectrometer (GC/MS) is generally used for analysis of furan in food samples. The risk assessment of furan can be characterized using margin of exposure approach (MOE). Conventional strategies including cooking in open vessels, reheating of commercially processed foods with stirring, and physical removal using vacuum treatment have remained unsuccessful for the removal of furan due to the complex production mechanisms and possible precursors of furan. The innovative food-processing technologies such as high-pressure processing (HPP), high-pressure thermal sterilization (HPTS), and Ohmic heating have been adapted for the reduction of furan levels in baby foods. But in recent years, only HPP has gained interest due to successful reduction of furan because of its nonthermal mechanism. HPP-treated baby food products are commercially available from different food companies. This review summarizes the mechanism involved in the formation of furan in foods, its toxicity, and identification in infant foods and presents a solution for limiting its formation, occurrence, and retention using novel strategies.

COVID-19 and diet: efforts towards a balanced diet and sustainable nutrition among university students in Pakistan.

Nutrition is an important aspect of a healthy lifestyle for all individuals, including adolescents. The objective of this cross-sectional descriptive survey study was to investigate university students' awareness of immunity enhancing foods, food nutritive values, and eating practices during the COVID-19 pandemic. A total of 839 university students from four different universities in Pakistan participated in the study from October 2021 to January 2022, 397 of which were male and 442 were female. A total of 419 students were studying in medical disciplines while 420 were non-medical students. The students had significant knowledge (p < 0.05) about COVID-19, and nutritional habits were seen in both medical and non-medical students. Results showed that medical students (n-201) were slightly more aware of immunity-enhancing foods and the nutritive values of foods compared to engineering students (n-79). However, eating practices were generally poorly adopted by all of the university students. Male and female students were not significantly different in their mean replies to questions on the nutritive value of food or in their eating habits. Healthy eating practices will aid university students in preventing illnesses connected to nutrition as well as enhancing their immune systems and nutritional well-being both during and post-pandemic. In light of these results, suggestions and implications for nutritional advice and education were explored.

Chondrocyte-specific regulatory activity of Runx2 is essential for survival and skeletal development.

Coordinated activities of multiple mesenchymal cell types contribute to the development of the mammalian skeleton formed through endochondral ossification. Synthesis of a cartilage template by chondrocytes is an obligatory step for the generation of skeletal elements during endochondral ossification. Gene ablation studies have established that Runx2 is an essential transcription factor for bone formation and the differentiation of skeletal cells. However, global gene deletion has failed to discern the tissue- and cell type-specific roles of Runx2. We generated floxed mice to elucidate the Runx2 regulatory control distinctive to cartilage tissue during bone development. Exon 8 of the Runx2 gene was selectively deleted in developing chondrocytes by utilizing Col2a-Cre mice. Cell- and tissue-specific gene recombination was confirmed by ß-gal activity in R26R mice. The chondrocyte-specific loss of Runx2 caused failure of endochondral ossification, impaired craniofacial development, dwarfism, and perinatal lethality. Radiographic imaging and histochemical approaches were used to characterize the skeletal phenotype. We conclude that regulatory control of Runx2 in chondrocytes is essential for endochondral ossification, and it is independent of the role of Runx2 in osteoblasts.

Runx2 regulates the gene network associated with insulin signaling and energy homeostasis.

Glucose intolerance seen in metabolic disorders, such as type II diabetes, is commonly associated with improper execution of the insulin signaling pathway, as well as an imbalance of bone and fat tissues, such that a gain in adipose tissue occurs at the expense of bone loss. Fat-producing adipocytes and bone-forming osteoblasts stem from a common mesenchymal progenitor cell. Runx2 positively regulates the commitment of the mesenchymal cell toward osteogenesis, but its effects on energy homeostasis and the insulin signaling pathway are unknown. To investigate the connection, focused microarray profiling of genes associated with the insulin signaling pathway was performed on calvarial cells from Runx2-null embryonic mice and 3T3-L1 preadipocytes treated with control and insulin-containing media. The microarray showed that addition of insulin resulted in a robust induction of genes (>95%) in 3T3-L1 cells. Surprisingly, Runx2-null cells cultured in control media were at an elevated state of energy metabolism and addition of insulin resulted in a marked suppression of genes required for insulin signaling. Clustering analysis revealed that the suppression occurred at all stages of the insulin pathway, from the receptors and transducers to nuclear effectors and target genes. Taken together, these results demonstrate that Runx2 is central for transduction and execution of the insulin regulatory signal. In conclusion, Runx2 actively regulates the gene network required for glucose metabolism and energy homeostasis in mesenchymal cells.

Runx2 regulates endochondral ossification through control of chondrocyte proliferation and differentiation.

Synthesis of cartilage by chondrocytes is an obligatory step for endochondral ossification. Global deletion of the Runx2 gene results in complete failure of the ossification process, but the underlying cellular and molecular mechanisms are not fully known. Here, we elucidated Runx2 regulatory control distinctive to chondrocyte and cartilage tissue by generating Runx2 exon 8 floxed mice. Deletion of Runx2 gene in chondrocytes caused failure of endochondral ossification and lethality at birth. The limbs of Runx2(ΔE8/ΔE8) mice were devoid of mature chondrocytes, vasculature, and marrow. We demonstrate that the C-terminus of Runx2 drives its biological activity. Importantly, nuclear import and DNA binding functions of Runx2 are insufficient for chondrogenesis. Molecular studies revealed that despite normal levels of Sox9 and PTHrP, chondrocyte differentiation and cartilage growth are disrupted in Runx2(ΔE8/ΔE8) mice. Loss of Runx2 in chondrocytes also impaired osteoprotegerin-receptor activator of NF-κB ligand (OPG-RANKL) signaling and chondroclast development. Dwarfism observed in Runx2 mutants was associated with the near absence of proliferative zone in the growth plates. Finally, we show Runx2 directly regulates a unique set of cell cycle genes, Gpr132, Sfn, c-Myb, and Cyclin A1, to control proliferative capacity of chondrocyte. Thus, Runx2 is obligatory for both proliferation and differentiation of chondrocytes.