Скачать с ютуб Organ failure mechanism in pancreatitis в хорошем качестве

Organ failure mechanism in pancreatitis

Visceral adipose tissue plays a critical role in numerous diseases. While imaging studies often show adipose involvement in abdominal diseases, their outcomes may vary from being a mild self limited illness to one with systemic inflammation and organ failure. We therefore compared the pattern of visceral adipose injury during acute pancreatitis and acute diverticulitis to determine its role in organ failure. Acute pancreatitis-associated adipose tissue had ongoing lipolysis in the absence of adipocyte triglyceride lipase (ATGL). Pancreatic lipase injection into mouse visceral adipose tissue hydrolyzed adipose triglyceride and generated excess non-esterified fatty acids (NEFA), which caused organ failure in the absence of acutepancreatitis. Pancreatic triglyceride lipase (PNLIP) increased in adipose tissue during pancreatitis and entered adipocytes by multiple mechanisms, hydrolyzing adipose triglyceride and generating excessive NEFA. During pancreatitis, obese PNLIP knockout mice, unlike obese adipocyte-specific ATGL knockouts, had lower visceral adipose tissue lipolysis, milder inflammation, lesser organ failure, and improved survival. PNLIP knockout mice, unlike ATGL knockouts, were protected from adipocyte-induced pancreatic acinar injury without affecting NEFA signaling or acute pancreatitis induction. Therefore during pancreatitis, unlike diverticulitis, PNLIP leaked into visceral adipose tissue can cause excessive visceral adipose tissue lipolysis independent of adipocyte-autonomous ATGL, and thereby worsen organ failure.