The Role of FTO Risk Haplotype in Overweight/Obesity and Lipid Parameters-Results From the Central China Population Study.

Fat mass and obesity-associated gene (FTO) genes rs9939609 is strongly associated with obesity and rs17817449 is an important and potential gene for obesity, have been well established. We aim to evaluate the relationship between FTO gene and overweight/obesity and confirm the influence of obesity on glucose and lipid metabolism parameters. We investigated 183 normal weight subjects and 193 individuals with overweight/obesity.

A case report of acute Q fever with low-read detection of Coxiella burnetii genome by next-generation metagenomic sequencing.

The case presents a 47-year-old man with sudden abdominal pain and fever, but the cause was uncertain. Through metagenomic next-generation sequencing (mNGS) and detecting Q fever antibodies in serum, along with the patient's clinical and epidemiological history, a precise diagnosis was made, enabling timely and proper treatment.

Salusin‑α alleviates lipid metabolism disorders via regulation of the downstream lipogenesis genes through the LKB1/AMPK pathway.

Lipid metabolism disorders are a major cause of several chronic metabolic diseases which seriously affect public health. Salusin‑α, a vasoactive peptide, has been shown to attenuate lipid metabolism disorders, although its mechanism of action has not been reported. To investigate the effects and potential mechanisms of Salusin‑α on lipid metabolism, Salusin‑α was overexpressed or knocked down using lentiviral vectors.

Overexpression of salusin‑β downregulates adipoR1 expression to prevent fatty acid oxidation in HepG2 cells.

Salusin‑β and adiponectin receptor 1 (adipoR1) serve important roles in the development of certain cardiovascular diseases and lipid metabolism. However, to the best of our knowledge, the relationship between salusin‑β and adipoR1, and their underlying mechanisms of action, currently remain unclear. In the present study, lentiviral vectors designed to overexpress salusin‑β or knock down salusin‑β expression were used in 293T and HepG2 cells.

Overexpression of salusin‑α upregulates AdipoR2 and activates the PPARα/ApoA5/SREBP‑1c pathway to inhibit lipid synthesis in HepG2 cells.

Salusin‑α and adiponectin, are vasoactive peptides with numerous similar biological effects related to lipid metabolism. Adiponectin has been shown to reduce fatty acid oxidation and to inhibit lipid synthesis of liver cells through its receptor, adiponectin receptor 2 (AdipoR2), but whether salusin‑α is able to interact with AdipoR2, was not previously reported. To investigate this, experiments were carried out.