The new emerging model for human diseases is the zebrafish (Danio rerio). Approximately 70% of the zebrafish genome matches the human genome, and 84 percent of human disease can be modelled in zebrafish. The ease of acquisition, breeding, and natural habitat are all factors that favour the use of zebrafish in animal research studies. Humans and zebrafish share similarities in the organogenesis and development of their cardiovascular, gastrointestinal, and nervous systems. Obesity is linked to the majority of human ailments, including diabetes, hypertension, cardiovascular disease, stroke, and osteoporosis, and it is also linked to a decline in cognitive functions in humans.

According to the WHO, 13% of the world’s population was obese in 2016, and the prevalence of obesity increased threefold between 1975 and 2016. In Southeast Asia, 6.6 million children under the age of five are overweight, and one out of every five adults is obese. In these countries, double malnutrition (undernutrition and obesity) is common. Obesity is the world’s sixth most important risk factor for many other diseases. Obesity, in addition to other health issues, can have an impact on cognitive and motor functions.

Zebrafish has proven to be an effective model for mammalian obesity in the study of various obesity-related diseases in humans.

Many studies have found similarities between the metabolic pathways of obese zebrafish and those of mammalian obesity. Oka et al. discovered that a diet-induced obesity zebrafish model shared pathophysiological mechanisms with mammalian obesity. Because of similarities with humans in the structure and functions of the pancreas, adipose tissue, lipid metabolism, and glucose homeostasis, zebrafish has replaced rodent models as an appealing animal model for the study of various metabolic disorders. Obese zebrafish have been shown to have cardiovascular overload changes similar to humans. Adult zebrafish have proven to be an effective model for metabolic disease research. This study focuses on developing a simple obesity model with limited resources that can be used for future experimentation on obesity-related research.

A reference range for zebrafish obesity parameters is required, which can be used for any zebrafish obesity studies. As a result, the goal of this study is to develop a simple zebrafish obesity model and calculate the average length, weight, and body mass index (BMI) of zebrafish aged 5–8 months.

Several metabolic studies have shown that the regional distribution of fat within the body is more important than total body fat in predicting the development of obesityrelated comorbidities. The amount of visceral adipose tissue (VAT) and ectopic fat deposition, in particular, are strongly linked to an increased risk of developing cardiovascular and metabolic disorders. These obesity related disorders are commonly referred to as metabolic syndrome, and they are found in the majority of obese people.

Obesity is a multifactorial disease that is influenced by both genetic and environmental factors. Obesity animal models are needed to help us understand the signalling pathways that underpin this condition. Because zebrafish have many structural and functional similarities with humans, they have been used to model a variety of human diseases, including a genetic model of obesity. The goal of this research was to create a zebrafish model of diet-induced obesity (DIO). Although the zebrafish has become popular in recent decades for basic biomedical research due to the numerous advantages highlighted in several articles, it has not been used extensively for obesity and diet studies. The first zebrafish studies on adipose tissue and obesity appeared in 2010, with data on the distribution of adipose white tissue in adult zebrafish under normal conditions. Furthermore, in live zebrafish larvae, a direct relationship between a fat-rich diet and adipocyte development was discovered. Oka and colleagues proposed a diet-induced obesity (DIO) protocol in adult zebrafish using a diet administered over a short period of time in 2010, and other groups proposed a test to evaluate obesity in larvae in 2011. They used Nile red, a vital dye that is incorporated into adipose tissue during tissue formation, for this. Both techniques are critical for studying this pathology in this model. Overnutrition, it was discovered in 2014, stimulates the formation of beta cells in the pancreas. Increasing the number of beta cells may favour hyperinsulinemia, and the excess insulin would induce metabolic changes favouring lipid accumulation in white adipose tissue. The metabolism of lipids in zebrafish is similar to that of mammals. Lipids are absorbed from dietary lipids and transported from the intestine to the liver, where they are distributed throughout the body. Lipoprotein carriers (VLDL, LDL, HDL) transport lipids in the blood in the same way that they do in mammals. In addition, zebrafish has an energy homoeostasis regulatory pathway that includes a central melanocortin system that responds to leptin. Adiponectin and adiponectin receptors, agouti-related protein, PPARs (peroxisomeproliferator-activated receptors), a lipid sensor and regulator of lipid metabolism, leptin, and the regulatory lipid synthesis pathway SCAP/SREBP have all been discovered in zebrafish. Obesogenic and antiobesogenic drugs have been tested successfully in this model, indicating that key regulatory pathways of adipogenesis in zebrafish are conserved.

The evidence supports the hypothesis of a relationship between high lipid content diets, obesogenic pathways dysregulation, and obesity; the findings appear to confirm the role of these two factors in the development of cardiovascular diseases and could be extrapolated to humans. The findings also highlight the importance of incorporating a balanced diet early in life to lower the risk of chronic, high-cost, and uncontrollable diseases in adults. Given the growing body of evidence, the DIO zebrafish model is regarded as a useful, low-cost model for studying the relationship between obesity and noncommunicable chronic diseases, clarifying trigger mechanisms, and proposing prevention and therapeutic actions. This data can then be used to support public health care programmes aimed at reducing the global burden of obesity-related diseases.