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Obesity is a complex chronic condition associated with multiple health risks, including visceral obesity, which is particularly detrimental. To gain insight into the mechanisms underlying obesity and its associated pathologies, a novel zebrafish model was established using an innovative high-fat diet (HFD). The primary goal was to induce visceral obesity in zebrafish and study the associated structural changes. To achieve this, a unique HFD consisting of 40% beef fat (HFD40) was developed and supplemented with magnesium aluminometasilicate to improve stability in a high humidity environment. Feeding regimens were initiated for both juvenile (starting at 2 weeks post-fertilization, lasting 18 weeks) and adult zebrafish (3 months post-fertilization, 8 weeks feeding duration). The innovative dietary approach successfully induced visceral obesity in both juvenile and adult zebrafish. This new model provides a valuable tool to study obesity-related pathologies, metabolic syndrome, and potential therapeutic interventions. Most importantly, the low-cost and easy-to-prepare composition of HFD40 was seamlessly incorporated into the water without the need for separation, was readily absorbed by the fish and induced rapid weight gain in the zebrafish population. In conclusion, this study presents a novel HFD40 composition enriched with a high beef fat concentration (40%), which represents a significant advance in the development of an experimental zebrafish model for the study of visceral obesity and associated metabolic changes., (© 2024. The Author(s).)

Acrylamide (ACR) is an amide formed as a byproduct in many heat-processed starchy-rich foods. In utero ACR exposure has been associated with restricted fetal growth, but its effects of postnatal functional development of small intestine is completely unknown. The current study investigated the time- and segment-dependent effects of prenatal ACR exposure on morphological and functional development of small intestine in weaned rat offspring. Four groups of pregnant female Wistar rats were exposed to ACR (3 mg/kg b.w./day) for 0, 5, 10 and 15 days during pregnancy. Basal intestinal morphology, immunolocalization of gut hormones responsible for food intake and proteins of intestinal barrier, activity of the intestinal brush border disaccharidases, apoptosis and proliferation in intestinal mucosa were analyzed in offspring at weaning (postnatal day 21). The results showed that in utero ACR exposure disturbs offspring gut structural and functional postnatal development in a time- and segment-depended manner and even a short prenatal exposure to ACR resulted in changes in intestinal morphology, immunolocalization of leptin and ghrelin and their receptors, barrier function, activity of gut enzymes and upregulation of apoptosis and proliferation. In conclusion, prenatal ACR exposure disturbed the proper postnatal development of small intestine., (© 2023. The Author(s).)