The polycystic ovary syndrome (PCOS) is defined as a combination of hyperandrogenism (hirsutism and acne) and anovulation (oligomenorrhea, infertility, and dysfunctional uterine bleeding), with or without the presence of polycystic ovaries on ultrasound. It represents the main endocrine disorder in the reproductive age, affecting 6% -15% of women in menacme. It is the most common cause of infertility due to anovulation, and the main source of female infertility. When in the presence of a menstrual disorder, the diagnosis of PCOS is reached in 30% -40% of patients with primary or secondary amenorrhoea and in 80% of patients with oligomenorrhea. PCOS should be diagnosed and treated early in adolescence due to reproductive, metabolic and oncological complications which may be associated with it. Treatment options include drugs, diet and lifestyle improvement.

Diabetes mellitus (DM) is considered a major public health problem because of its high prevalence and progressive increase of incidence. DM chronic complications are major causes of morbidity and mortality, among which diabetic neuropathy (DN) stands out, affecting 30% -50% of DM patients. An appropriate medical approach, involving anamnesis and thorough clinical examination, is extremely important for the early diagnosis of DN and, therefore, to the prevention of its complications, including the amputation of limbs. Despite of the importance of DN prevention and treatment, in order to provide improved quality of life and longevity to DM patients, current therapeutic options are very limited with respect to both symptom control and as effective disease therapies. Intensive glucose control is extremely important in order to prevent and avoid the progression of DN, as demonstrated in two large multicenter studies involving patients with type 1 DM, the DCCT (Diabetes Control and Complications Trial) and the EDIC (Epidemiology of Diabetes Interventions and Complications).

Obesity is a disease of epidemic proportions, associated with chronic inflammation in response to increased secretion of inflammatory cytokines originating in adipose tissue. Exercise has been shown to be effective in combating these changes. The aim of this study was to review the anti-inflammatory effect of physical exercise in the pathogenesis of obesity. We conducted a search of the terms "exercise", "obesity" and "inflammation" on Medline and PubMed databases, restricting results to clinical trials published since 2011. The retrieved studies showed that physical exercise could, via different pathways, reduce levels of CRP, IL-6 and TNF-α, as well as other proinflammatory markers. Additionally, exercise was able to increase expression of genes related to the production of nitric oxide, positively modulating endothelial function and chronic inflammation in obese patients, with or without caloric restriction. In conclusion, aerobic exercise of moderate intensity is an effective intervention strategy for chronic inflammation associated with obesity.

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In type 1 diabetes mellitus (T1DM), growth hormone (GH) responses to provocative stimuli are normal or exaggerated, whereas the hypothalamic-pituitary-adrenal axis has been less studied. Ghrelin is a GH secretagogue that also increases adrenocorticotropic hormone (ACTH) and cortisol levels, similarly to GH-releasing peptide-6 (GHRP-6). Ghrelin's effects in patients with T1DM have not been evaluated. We therefore studied GH, ACTH, and cortisol responses to ghrelin and GHRP-6 in 9 patients with T1DM and 9 control subjects. The GH-releasing hormone (GHRH)-induced GH release was also evaluated. Mean fasting GH levels (micrograms per liter) were higher in T1DM (3.5 ± 1.2) than in controls (0.6 ± 0.3). In both groups, ghrelin-induced GH release was higher than that after GHRP-6 and GHRH. When analyzing Δ area under the curve (ΔAUC) GH values after ghrelin, GHRP-6, and GHRH, no significant differences were observed in T1DM compared with controls. There was a trend (P = .055) to higher mean basal cortisol values (micrograms per deciliter) in T1DM (11.7 ± 1.5) compared with controls (8.2 ± 0.8). No significant differences were seen in ΔAUC cortisol values in both groups after ghrelin and GHRP-6. Mean fasting ACTH values were similar in T1DM and controls. No differences were seen in ΔAUC ACTH levels in both groups after ghrelin and GHRP-6. In summary, patients with T1DM have normal GH responsiveness to ghrelin, GHRP-6, and GHRH. The ACTH and cortisol release after ghrelin and GHRP-6 is also similar to controls. Our results suggest that chronic hyperglycemia of T1DM does not interfere with GH-, ACTH-, and cortisol-releasing mechanisms stimulated by these peptides.