There is a general consensus that a reduction in growth hormone (GH) secretion results in obesity. However, the pathophysiologic role of GH in the metabolism of lipids is yet to be fully understood. The major somatic targets of GH are bones and muscles, but GH stimulates lipolysis and seems to regulate lipid deposition in adipose tissue. Patients with isolated GH deficiency (GHD) have enlarged fat depots due to higher fat cell volume, but their fat cell numbers are lower than those of matched controls. The treatment of patients with GH results in a relative loss of body fat and shifts both fat cell number and fat cell volume toward normal, indicating an adipogenic effect of GH. Adults with GHD are characterized by perturbations in body composition, lipid metabolism, cardiovascular risk profile, and bone mineral density. It is well established that GHD is usually accompanied by an increase in fat accumulation; GH replacement in GHD results in the reduction of fat mass, particularly abdominal fat mass. In addition, abdominal obesity results in a secondary reduction in GH secretion that is reversible with weight loss. However, whereas GH replacement in patients with GHD leads to specific depletion of intra-abdominal fat, administering GH to obese individuals does not seem to result in a consistent reduction or redistribution of body fat. Although administering GH to obese non-GHD subjects has only led to equivocal results, more recent studies indicate that GH still remains a plausible metabolic candidate.

Introduction: Leprosy is an infectious disease whose etiologic agent is Mycobacterium leprae. Despite its notoriety, there are mechanisms of molecular interaction that have not been elucidated. Therefore, it was carried out a literary review about the molecular interaction between M. leprae and the Schwann cell (SC), characterizing the mechanisms of endocytosis and cellular damage. Methods: It was delimited a 10-year timeframe (2010 to 2020). The research bases used were Portal de Periódicos CAPES/MEC, National Library of Medicine - PubMed, World Health Organization (WHO) Statistical Data, Pan American Health Organization (PAHO), Ministry of Health of Brazil Data, Scielo, Fundação Oswaldo Cruz (ARCA-FIOCRUZ) and UpToDate Inc. Results: M. Leprae is endocitized through interactions with basal lamina of the SC, whose α-laminin 2 enables the formation of the dystrophin-dystroglycan complex. Moreover, the activity of the pathogen in the SC is associated with direct, indirect and additional damage. It was verified the need for continuous studies due to the complexity of this molecular biointeraction, given the cellular reprogramming of SC and its neuronal impact. Conclusion: There are still many scientific gaps, requiring further clarification in the area, which results in uncertainties in the tropism of the pathogen with the peripheral nerves.