the closest moment to my death , After consuming 7 bottles of beer, I began to feel bloated, sweating profusely, and pain in my stomach, back, and waist. Ibuprofen didn’t work. I vomited to the point of sour water and bile.
When I was sent to the emergency room, I was so weak that I was almost semi-conscious, After blood test and CT examination, I was diagnosed with severe acute pancreatitis. I stayed in the ICU for a month, spent more than 100,000 before and after, and barely saved my life. I still feel scared…< /span>
Severe acute pancreatitis induced by heavy drinking almost broke the ICU, and Not a single case, acute pancreatitis is the most common digestive system emergency, 20% of patients will develop moderate to severe acute pancreatitis, and in the case of multiple organ disorders, the mortality rate is as high as 20%-40%.
Alcoholismis the main cause of acute pancreatitis after gallstones. The intake is closely related to the increased incidence of acute pancreatitis.
The problem is that even among heavy drinkers, only 2% to 3% develop acute pancreatitis, suggesting that alcohol may It is not the direct cause of acute pancreatitis, and other factors play a role in this process.
Recently, a study published in Gut by Xia Qing, Huang Wei and their team from West China Hospital of Sichuan University revealed that
span>Obesity is an important synergistic factor of alcohol-induced severe acute pancreatitis. Large intake of alcohol induces visceral lipolysis to release free fatty acids（free fatty acids, FFAs） is the key to pancreatic injury and multiple organ dysfunction.
In this experiment, the research subjects were mainly obese mice fed with high-fat diet and slender mice fed with standard chow.
After 12 weeks of high-fat/standard diet, mice were intraperitoneally injected with 37.5% ethanol solution at a dose of 2 g/kg , 2 consecutive injections with a time interval of 1 hour to construct a mouse model of severe acute pancreatitis.
3-6 hours after alcohol injection in obese mice The pancreatic tissue rapidly developed edema, inflammation and necrosis, peripheral blood pancreatin, pancreatic and lung myeloperoxidase increased, serum IL-6 level increased, and multiple organ damage index increased, and all disease indicators peaked after 12 hours .
However, unlike obese mice, slim mice only developed mild pancreatic edema after alcohol injection, without any severe acute The manifestations of pancreatitis indicate that alcohol cannot make the slim mice have obvious manifestations of acute pancreatitis.
abdominal and autopsy results of alcohol-injected obese mice Fat saponification occurred around the pancreas (free fatty acid combined with calcium ions to produce saponification). The researchers believe that these free fatty acids are mainly derived from alcohol-induced lipolytic release of visceral adipose tissue in obese mice.
Adipose triglyceride lipase in freshly isolated epididymal adipose tissue from obese mice 3 hours after alcohol injection(adipose triglyceride lipase, ATGL) content increased, and the release of triglyceride breakdown products – free fatty acids and glycerol was greatly increased, while in lean mice before and after alcohol injection, fat triglyceride Lipase and free fatty acid content did not change significantly.
Next, to explore whether these free fatty acids released from visceral adipose tissue are the key to alcohol-induced severe acute pancreatitis, the researchers Injecting alcohol and adipocytes from obese mice into the abdominal cavity of lean mice successfully reproduced the performance of severe acute pancreatitis in obese mice in lean mice, but neither alcohol nor adipocytes alone were sufficient to induce The occurrence of severe acute pancreatitis.
In other words, only when alcohol and adipose tissue are hydrolyzed to release free fatty acids Severe acute pancreatitis can only occur under the combined action.
In conclusion, this study demonstrates for the first time that obesity plays a synergistic role in the development of alcohol-induced acute pancreatitis, and the hydrolysis of visceral fat releases a large amount of Free fatty acids are also the trigger for the progression of the disease to severe pancreatitis.
It seems that obese people need to weigh their stomachs and think twice before drinking alcohol.
References[1]Yang X, Yao L, Dai L, et al. Alcohol predisposes obese mice to acute pancreatitis via adipose triglyceride lipase-dependent visceral adipocyte lipolysis [published online ahead of print, 2022 Apr 22]. Gut. 2022;gutjnl-2022-326958. doi:10.1136/gutjnl-2022-326958 [2]Boxhoorn L, Voermans RP, Bouwense SA, et al. Acute pancreatitis [published correction appears in Lancet. 2021 Nov 6;398(10312):1686]. Lancet. 2020;396(10252):726- 734. doi:10.1016/S0140-6736(20)31310-6[3]Samokhvalov AV, Rehm J, Roerecke M. Alcohol Consumption as a Risk Factor for Acute and Chronic Pancreatitis: A Systematic Review and a Series of Meta-analyses. EBioMedicine. 2015;2(12):1996-2002. Published 2015 Nov 14. doi:10.1016/j.ebiom.2015.11.023
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