Metabolic Derangement in Pediatric Patient with Obesity: The Role of Ketogenic Diet as Therapeutic Tool.

Obesity is defined as a condition characterized by an excessive fat accumulation that has negative health consequences. Pediatric obesity is associated with an increased risk for many diseases, including impaired glycemic and lipidic control that may lead to the development of chronic, and potentially disabling, pathologies, such as type 2 diabetes mellitus (T2DM) and cardiovascular events, in adult life. The therapeutic strategy initially starts with interventions that are aimed at changing lifestyle and eating behavior, to prevent, manage, and potentially reverse metabolic disorders. Recently, the ketogenic diet (KD) has been proposed as a promising dietary intervention for the treatment of metabolic and cardiovascular risk factors related to obesity in adults, and a possible beneficial role has also been proposed in children. KD is very low in carbohydrate, high in fat, and moderate to high in protein that may have the potential to promote weight loss and improve lipidic derangement, glycemic control, and insulin sensitivity. In this review, we present metabolic disorders on glycemic and lipidic control in children and adolescents with obesity and indication of KD in pediatrics, discussing the role of KD as a therapeutic tool for metabolic derangement. The results of this review may suggest the validity of KD and the need to further research its potential to address metabolic risk factors in pediatric obesity.

Polycystic Ovary Syndrome in Insulin-Resistant Adolescents with Obesity: The Role of Nutrition Therapy and Food Supplements as a Strategy to Protect Fertility.

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in young reproductive-aged women. PCOS is often associated with obesity and impairs reproductive health. Even though several theories have been proposed to explain the pathogenic mechanism of PCOS, the role of insulin resistance (IR) as a key etiological component, independently of (but amplified by) obesity, is well recognized. The consequent hyperinsulinemia activates excessive ovarian androgen production, leading to PCOS. Additionally, the state of chronic inflammation related to obesity impacts ovarian physiology due to insulin sensitivity impairment. The first-line treatment for adolescents with obesity and PCOS includes lifestyle changes; personalized dietary interventions; and, when needed, weight loss. Medical nutrition therapy (MNT) and the use of specific food supplements in these patients aim at improving symptoms and signs, including insulin resistance and metabolic and reproductive functions. The purpose of this narrative review is to present and discuss PCOS in adolescents with obesity, its relationship with IR and the role of MNT and food supplements in treatment. Appropriate early dietary intervention for the management of adolescents with obesity and PCOS should be considered as the recommended approach to restore ovulation and to protect fertility.

Insulin resistance and potential modulators of ovarian reserve in young reproductive-aged women with obesity and type 1 diabetes.

INTRODUCTION: Both obesity and diabetes play a significant role in reproductive disorders in women and insulin resistance (IR) is a confirmed trait d'union. We evaluated the relationship between IR and an established ovarian reserve biomarker such as anti-mullerian hormone (AMH) together with other potential modulators of ovarian physiology (adiponectin and kisspeptin) in young reproductive-aged group women with obesity and type 1 diabetes (T1D). PATIENTS AND METHODS: We recruited 32 female youths: 14 of them presented with T1D (14.6 ± 2.6 years) and 18 with obesity (15.1 ± 2.6 years). The control group included 20 age-matched normal weight females. Each patient underwent physical examination and hormonal assessment. AMH, kisspeptin and adiponectin levels were also measured. IR was calculated as the homeostasis model assessment for insulin resistance (HOMA-IR) and the glucose disposal rate (eGDR) in patients with obesity and with T1D, respectively. RESULTS: adiponectin and kisspeptin levels were significantly different into groups (p ≤ .001), whereas AMH levels were not. Adiponectin values were higher in controls compared to patients with obesity (p < .001) and T1D (p = .02). Kisspeptin levels were lower in controls compared to patients with obesity (p = .001), without reaching statistical significance when compared to T1D (p = .06). IR was associated with lower adiponectin and higher kisspeptin levels (p < .001 and p = .02, respectively), but not with AMH. CONCLUSIONS: IR displays a relationship with adiponectin and kisspeptin in young reproductive-aged women with obesity and T1D. Interventions to correct IR in adolescents could be part of an early approach to prevent reproductive disorders and to promote factors associated with longevity in adult women.