In endemic areas, schistosomiasis, caused by Platyhelminthes Trematodes of the genus Schistosoma spp., has high morbidity and mortality rates and a high prevalence worldwide, with an estimated 250 million people infected and 3.3 million disability-adjusted life years lost. Schistosoma mansoni plays the leading role in cases of this disease, particularly in Africa and South America [1].

In endemic areas, schistosomiasis, caused by Platyhelminthes Trematodes of the genus Schistosoma spp., has high morbidity and mortality rates and a high prevalence worldwide, with an estimated 250 million people infected and 3.3 million disability-adjusted life years lost. Schistosoma mansoni plays the leading role in cases of this disease, particularly in Africa and South America [1].

This trematode is highly dependent on the host's metabolism due to its strict hematophagous nature. In this regard, it is noted that the parasite's dependence on its human host is so pronounced that host particles such as tumor necrosis factor and interleukin-7, and even thyroid hormones, play a role in the growth and fecundity of these parasites, as they can disrupt oviposition or interfere with the development of the adult parasite [2, 3].

Receptors in the basement membrane of the tegument and muscle of the adult parasite, specifically insulin receptors, allow the uptake of glucose necessary for the parasite's growth and metabolism—essential biological processes for its survival. Therefore, it is valid to ask whether the growth and reproduction of Schistosoma spp. is negatively affected in human hosts with type 1 diabetes mellitus (T1DM), a metabolic disorder characterized by poor or absent insulin production? [3, 4].

On the one hand, T1DM favors microbial infections, and on the other, it limits parasitic infections. This latter idea, although highly probable, still requires scientific confirmation. However, it is postulated that the cellular immune response against the parasite's eggs is impaired in patients with T1DM, generating small granulomas surrounding the eggs in the liver and intestine (resulting in reduced protection), as well as impaired egg maturation and reduced excretion in feces [3, 5, 6].

Process, in relation to the limitation of the survival of the trematode, attacked by the parasite itself with the deviation of the immune response from Th1 to Th2, since it is known that DM1 is an autoimmune disease mediated by Th1 cells (due to prolonged production of IL-4, IL-5, IL-10 and TGFβ), as demonstrated by studies carried out in non-obese diabetic mice exposed to soluble antigens of S. mansoni eggs, therefore, the success of one pathology over the other in the comorbidity of DM1 and schistosomiasis seems to be due to a delicate balance [3, 7].

Another aspect to note, but as a risk factor for the development of diabetes mellitus in the parasite-host dyad, is obesity (resulting from the imbalance between food intake, basal metabolism, and energy expenditure [lower in sedentary lifestyles and physical inactivity]), which inevitably leads to insulin resistance and impaired pancreatic beta-cell function due to increased levels of non-esterified fatty acids, cytokines, hormones, glycerol, and pro-inflammatory markers [3, 8-10].

Being obese can contribute to the parasite's survival, because cholesterol is essential in modulating the parasite's cell signaling and reproduction (egg-laying rate), particularly since mature Schistosoma spp. cannot synthesize fatty acids de novo. It is believed that, through the consumption of fatty acids, the trematode may protect humans from the complications of obesity (reduction of lipid accumulation in blood vessels and control of type 2 diabetes), but with the inevitable increase in liver fibrosis caused by the parasite's presence in this organ [11-14].

This paper briefly but consistently presents the aspects involved in the interaction between S. mansoni and metabolic disorders, such as diabetes mellitus and obesity, based on immunological, histopathological, and biochemical parameters derived from non-human animal experiments, with the firm purpose of identifying the mechanisms involved in the pathology of these comorbidities.

Conflict of interests 

The authors have no conflict of interest to declare. The authors declared that this study has received no financial support.