Skinny fat model of metabolic syndrome induced by a high-salt/sucrose diet in young male rats.

Childhood and puberty can affect metabolism, leading to tissue injury and malfunction later in life. The consumption of high-processed foods rich in salt and sugar is increasing in middle- and high-income countries, especially among young people. It is necessary to evaluate the effects of high salt and sugar levels in the youth on most injured organs during metabolic challenges. We aimed to investigate whether high-salt/sucrose intake affects whole-body development and leads to end-organ injury. Weaned male Wistar rats were divided into two groups: a control group fed a standard diet and tap water, and an experimental group (SS) fed a standard diet and a beverage containing 1·8 % NaCl and 20 % sucrose instead of tap water. The animals were treated for 60 d, starting after weaning at 21 d of age, after which the animals were subjected to glucose and insulin tolerance tests, urine collection and heart rate monitoring and euthanised for sample collection at 81 d of age. SS showed reduced body weight gain and increased food intake of sodium/sucrose solution. Interestingly, high-salt/sucrose intake led to increased body adiposity, liver lipid inclusion, heart rate and renal dysfunction. SS exhibits increased levels of PPAR alpha to counterbalance the hypertrophy of brown adipose tissue. Our findings reveal that the SS rat model exhibits non-obvious obesity with end-organ damage and preserved brown adipose tissue function. This model closely parallels human conditions with normal BMI but elevated visceral adiposity, providing a relevant tool for studying atypical metabolic disorders.