Nowadays, obesity is seriously threatening healthy life in all societies, especially in developed societies. Obesity is showing its likely effects through biologically active substances called adipokines. The most familiar of these is leptin. Leptin is synthesized in directly proportional to the amount of adipose tissue and reduced appetite by stimulating the satiety center. This status is like a protective mechanism that tries to reverse severe pathological process. Similar to this behavior of leptin, thyroid hormones are increasing in the advanced stages of obesity, increasing the resting energy expenditure (REE). The accelerating oxidative phosphorylation causes the use of energy as heat, the energy that has not transformed into ATP, together with ATP synthesis. This situation, the significant portion of energy provides to consumed instead of storing as fat. In addition, finding that T3 accelerates glucose transport and the TCA cycle without changing the rate of ATP synthesis in skeletal muscles suggests that thyroid hormones may be an effective tool in standing against obesity. In addition of that, the presence of studies indicating that thyroid hormones have an increasing tendency in the advanced stages of obesity is likely thought to be a rescuer mechanism to increase the effectiveness of suppressed thyroid hormones. On the contrary of these ideas, having been reported suppressing 5’-deiodinease enzyme activity in chronic diseases causes anxiety about the effectiveness of thyroid hormones in obesity. Based on available information, we aimed to prepare a review evaluating of this adaptive condition of thyroid hormones. Show less

In literature, it has been reported that adrenomedullin, which is generally thought to have vasodilator, natriuretic and diuretic effects, is synthesized in almost all body, especially CNS, vascular muscles and endothelium, heart, liver, lung, kidney, gastric mocosa, intestinal endothelium and various blood cells. It has been found that the possible effects of adrenomedullin can be demonstrated directly or indirectly by means of active mediators, neuropeptides, enzymes and hormones. It is also suggested that it regulates the endocrine system by affecting the hypothalamic-pituitary axis. It increases in heart failure, acute coronary syndromes, hypertensive conditions, cerebrovascular accessory, chronic renal failure and periodontitis and decreases in peptic ulcer and intestinal diseases. However, it is still not clear whether increase/decrease in adrenomedullin level is a cause of a disease or is a result of damage due to an illness. This peptide, which could be thought to multifunctional, should be considered as a molecule with genetic coding that may have different effects on different tissues and conditions. For all these reasons, we aimed to review the multifonctional behavior of adrenemedullin in the light of the current literature to pioneer new hypotheses and discuss possible mechanisms. Show less

Brucella species cause a high burden of disease globally, infecting both humans and animals; however, One Health has been under-appreciated in Colombia. This study aimed to determine the seroprevalence of Brucella spp. in two remote indigenous communities from the Sierra Nevada de Santa Marta, Colombia. These communities live in close contact with their livestock, indicating a potential susceptibility to zoonotic pathogens. The livestock routinely kept by these communities include cattle, small ruminants and pigs, the known hosts of human pathogenic Brucella spp.. A low level of exposure to Brucella spp. was documented, with only one positive participant among 539 participants (0.2%; 95% CI 0.0 – 1.0). Nevertheless, due to the high risk that zoonoses pose, we recommend discussions with the community for the potential establishment of One Health surveillance studies for the early detection and prevention of future zoonotic disease threats. Show less

A sequence variation (I148M) in the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene has been linked to metabolic dysfunction-associated steatotic liver disease (MASLD) and the progression of MASLD and other chronic liver diseases towards fibrosis and cancer. To elucidate the role of PNPLA3 in metabolic liver injury, cholestasis or liver fibrosis, we utilized Pnpla3 knockout (KO) mice and investigated the impact of PNPLA3 deficiency on the inflammatory, cholestatic, and fibrotic phenotypes induced by MCD diet, bile duct ligation (BDL), 3,5-diethoxycarbonyl-1,4-dihydrocollidin (DDC) diet and carbon tetrachloride (CCl4), respectively. Upon MCD feeding, Pnpla3 KO and WT mice lost comparable amounts of white adipose tissue and showed similar degrees of liver injury. In addition, a down-regulation of genes regulating fatty acid oxidation was observed in Pnpla3 KO mice under chow diet, while no differences between experimental groups were seen in the expression of genes regulating fatty acid import, export, oxidation and de novo lipogenesis upon MCD feeding. Liver serum enzyme levels, fibrosis or cholestatic markers and inflammatory genes were not different between Pnpla3KO and WT mice after BDL. Markers of fibrosis, inflammation and biliary damage increased at the mRNA levels in response to DDC-induced cholestatic injury, without differences between WT and KO mice. Collagen deposition and hepatic fibrotic marker expression were similarly increased in CCl4 treated WT and Pnpla3 KO mice. Serum liver enzymes also increased upon CCL4 treatment without differences between WT and KO mice. In summary absence of Pnpla3 has no impact on the development of fatty liver, inflammation, cholestatic liver and bile duct injury, or hepatic fibrosis in mice. Show less