Background
Childhood obesity is a health problem that is difficult to manage because the obesogenic environment hinders long-term adherence to a diet. Eating behavior and energetic balance are controlled by neural circuits in the hypothalamic and hindbrain centers, which have afferent pathways related to sensory and hedonic centers, metabolic hormones and nutrient and adiposity signals.
Several programs of caloric restriction have been designed. Among them, carbohydrate or lipid restrictions have been used extensively with limited long-term results. In children, carbohydrate restriction offers a satisfactory weight loss and improvement of adiponectin levels. Lipid restriction may improve cardiometabolic risk factors such as triglycerides, low density lipoprotein cholesterol (LDL) and insulin levels. Lipid restriction may also improve Homeostatic Model Assessment- Insulin Resistance (HOMA-IR) scores, and leptin and proinflammatory cytokines levels regardless of body weight.
In obese children, low-carbohydrate (L-CHO) diet may induce a better improvement of HOMA-IR and triglyceride levels compared to lipid restriction; however, other reports have indicated that a low-fat (L-F) diet results in a better improvement of triglyceride levels.
For a better understanding of the effects of both types of macronutrient restriction, the impact on appetite-satiety mechanisms should be assessed. The Children's Eating Behavior Questionnaire (CEBQ) is a validated tool to identify diverse signals related to satiety, enjoyment of food, response to different foods, and emotional components of appetite-satiety physiology in children.
In children food intake and attitudes toward meals, depend on maternal influences. Maternal feeding restriction is associated with a child's food approach traits and responsiveness to food; however, appetitive traits may respond differently to dietary restriction of carbohydrates or fats, and to our knowledge this subject has not been studied in children.
Leptin and fibroblast growth factor 21 (FGF21) are related to the regulation of food ingestion and energetic balance. Leptin is a key appetite-regulating hormone produced in the white adipose tissue that acts on the hypothalamus. Leptin suppresses food intake and increases energy expenditure by means of adrenergic stimulation and stimulates peripheral fat oxidation and influences in glucose homeostasis by direct action on the pancreatic β cells. Therefore, deficiency of leptin or its receptors facilitates obesity, increases insulin resistance and impairs glucose tolerance. In humans, a diet with fat and carbohydrate restriction decreases leptin levels.
FGF21 is a product of the liver and adipose tissue with important roles in food intake, and energy expenditure. FGF21 mediates the metabolic response to starvation. FGF21 enhances insulin sensitivity, decreases triglyceride concentrations, and ameliorates obesity-associated hyperglycemia and hyperlipidemia. FGF21 also represses de novo lipogenesis by mediation of sterol regulatory element binding protein 1c transcription. FGF21 is proposed as a mediator of glucagon regulation of glucose and lipid metabolism and is an independent predictor of the metabolic syndrome in adults but not in children.
In animal models, the effect of a L-CHO diet on FGF21 levels is controversial. In mice, a L-CHO diet increases as an adaptive response to malnutrition; however, in another study FGF21 levels did not change. In adults, overfeeding increases FGF21 levels, and an acute response was found with a fructose load.
In obese children who participated in exercise, behavior, and nutrition therapy over the course of 1 year, body mass index (BMI) diminution was accompanied by a decrease in FGF21 levels; however, FGF21 did not change in adults on a ketogenic diet.
Surgical interventions in obese adults with intragastric balloon, laparoscopic sleeve gastrectomy or gastric banding decreases BMI and FGF21 levels; however in other studies, FGF21 levels did not change after intervention.
Carbohydrate or fat restrictions in the diet are strategies used to treat obesity with conflicting effects on appetite and satiety. Nevertheless, the effect on hormone and metabolic factors and the impact on long-term eating behavior are not well defined. Therefore, we examined the effect of restriction of carbohydrates or lipids, on diverse aspects of eating behavior and the metabolic and hormonal responses including leptin and FGF21 levels.