Hyperinsulinemia and insulin resistance are the common underlying physiopathological mechanisms for chronic metabolic disorders. Both overweight and obesity lay the foundation for the etiology of chronic metabolic disorders. The carbohydrate-insulin model indicates a high carbohydrate intake rises blood glucose level and promotes insulin secretion. Energy is stored as fat in adipose tissue under the direction of insulin. Consequently, the oxidation by metabolically active tissues is suppressed which leads to a cellular starvation state. In response, hunger and appetite are elevated and that results in an increased body weight. Restricting the dietary carbohydrate to 150g/d or below, or <26% of the total daily energy intake, decreases the insulinsecretion, and it could change how the body utilizes energy to promote the oxidation of fat. The alteration may lead to a decreased body weight due to the loss of fat mass. The low-carbohydrate diet puts no restriction on total energy and protein intake; therefore, it has better compliance comparing with other dietary interventions. The short-term efficacy of low-carbohydrate diets is evident in previous literature since it has fewer adverse health effects than drugs, and it is also cost-efficient regrading health economics. The low-carbohydrate diet is viewed as the first approach for managing chronic metabolic disorders including obesity, type 2 diabetes,NAFLD, and metabolic syndrome. Therefore, the research into low-carbohydrate diets is of great importance. However, low-carbohydrate diets should not be employed as an everyday diet under normal physiological state, and further research on its long-term effect is warranted.