The role of comorbid hypertriglyceridemia and abdominal obesity in the severity of acute pancreatitis: a retrospective study

Yang, Xiaoxi; He, Jiajun; Siddique, MA; Wang, Tingting; Zhu, Quping; Cao, Fei; Li, Yuanhao; Yang, Chuting; Chen, Chaowu; Lu, Guotao; Hu, Liang‐Hao; Li, Jun; Chen, Weiwei

doi:10.1186/s12944-021-01597-4

Cited by 17 publications

(14 citation statements)

References 35 publications

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“…29 In contrast, males contributed to approximately 50% of AP from other etiologies, wherein their average age were 10 years higher than in HTG-AP group. Similarly, a recent large study from China 31 conducted between 2016 and 2020 with 614 patients with HTG-AP reported that approximately 70% of the patients were males and the average age of presentation was in the mid-40s. Again, the age of presentation with non-HTG-AP was significantly higher, with an average of 60 years and males comprising 43%-52% of the non-HTG-AP group.…”

Section: Demographicsmentioning

confidence: 87%

Mechanisms linking hypertriglyceridemia to acute pancreatitis

et al. 2023

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Hypertriglyceridemia (HTG) is a metabolic disorder, defined when serum or plasma triglyceride concentration (seTG) is >1.7 mM. HTG can be categorized as mild to very severe groups based on the seTG value. The risk of acute pancreatitis (AP), a serious disease with high mortality and without specific therapy, increases with the degree of HTG. Furthermore, even mild or moderate HTG aggravates AP initiated by other important etiological factors, including alcohol or bile stone. This review briefly summarizes the pathophysiology of HTG, the epidemiology of HTG‐induced AP and the clinically observed effects of HTG on the outcomes of AP. Our main focus is to discuss the pathophysiological mechanisms linking HTG to AP. HTG is accompanied by an increased serum fatty acid (FA) concentration, and experimental results have demonstrated that these FAs have the most prominent role in causing the consequences of HTG during AP. FAs inhibit mitochondrial complexes in pancreatic acinar cells, induce pathological elevation of intracellular Ca2+ concentration, cytokine release and tissue injury, and reduce the function of pancreatic ducts. Furthermore, high FA concentrations can induce respiratory, kidney, and cardiovascular failure in AP. All these effects may contribute to the observed increased AP severity and frequent organ failure in patients. Importantly, experimental results suggest that the reduction of FA production by lipase inhibitors can open up new therapeutic options of AP. Overall, investigating the pathophysiology of HTG‐induced AP or AP in the presence of HTG and determining possible treatments are needed.

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Section: Demographicsmentioning

confidence: 87%

Mechanisms linking hypertriglyceridemia to acute pancreatitis

et al. 2023

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“…Although the age with non–HTG-AP was significantly higher, with an average of 60 years and males comprising 43% to 53% of the non–HTG-AP group. [20] Overall, the typical age of patients with HTG-AP is middle-aged and males are much more exposed than females.…”

Section: Epidemiology and Demographicsmentioning

confidence: 99%

Hypertriglyceridemia and acute pancreatitis: clinical and basic research—a narrative review

Gao,

2023

Journal of Pancreatology

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Hypertriglyceridemia (HTG) is the third most common cause for acute pancreatitis (AP), and the incidence of hypertriglyceridemia induced acute pancreatitis (HTG-AP) is rising worldwide as a result of changes in lifestyle and dietary habits. In China, HTG accounts for 10-20% the causes of AP, even becoming the second leading cause of AP. The presentation and diagnosis of HTG-AP is similar to that of AP from other causes, however, the complication rates and severe AP are significantly higher in patients with HTG-AP than in patients with other etiologies. Regarding the management for HTG-AP, the initial management is similar to that of AP from other causes and mainly includes fluid resuscitation, pain control and nutritional support. In addition to supportive care, it is necessary to take appropriate measures to decrease serum TG levels, in order to alleviate the progression of AP and prevent recurrence. This review aims to summarize existing clinical and basic research evidence of HTG-AP, and seeks to highlight the epidemiology, definition, pathogenesis, clinical course, diagnosis, management, prevention of recurrence and specific clinical scenarios, such as HTG-AP during pregnancy, HTG-AP with diabetic ketoacidosis.

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“…The mechanism via which obesity leads to SAP has been a topic of study for ages. Hypertriglyceridemia is an independent risk factor for local complications and persistent organ failure [11,12] . Pancreatic lipases can induce the lipolysis of adipocyte triglycerides to non-esteri ed free fatty acids (NEFA).…”

Section: Introductionmentioning

confidence: 99%

Activation of AMPK Ameliorates Acute Severe Pancreatitis by Suppressing Pancreatic Acinar Cell Necroptosis in Obese Mice Models

Yang

Wang

Zhao

et al. 2023

Preprint

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Obese people with acute pancreatitis(AP) have an increased risk of developing severe acute pancreatitis (SAP), which prolongs the length of hospital stay and increases mortality. Thus, elucidation of the mechanisms through which severe acute pancreatitis occurs in obese individuals will provide clues for possible treatment targets. Differences in early events in obese or lean patients with acute pancreatitis have not been conclusively reported. We selected C57BL/6 mice as lean mice models, ob/ob mice or diet induced obese (DIO) mice as obese mice models and then induced experimental AP in mice via injections of caerulein. There were suppressed p-AMPK expressions in the pancreas of obese mice, compared with same age lean C57BL/6 mice, which were further reduced in AP mice models. Obese AP mice were treated using AICAR, a direct AMPK agonist, which prevented pancreatic damage and cell death, suppressed pancreatic enzyme levels in serum, reduced the areas of fat saponification in the peritoneal cavity, prevented injury in other organs and decreased mice mortality rate. Further assays showed that AICAR activates p-AMPK to stabilize pro-caspase-8. Pro-caspase-8 enhances RIPK3 degradation, inhibits pancreatic acinar cell necroptosis and downregulates the release of pancreatic enzymes. Thus, activation of AMPK by AICAR alleviates pancreatic acinar cell necroptosis and converts SAP to mild acute pancreatitis (MAP) in obese mice.

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The role of comorbid hypertriglyceridemia and abdominal obesity in the severity of acute pancreatitis: a retrospective study

Cited by 17 publications

References 35 publications

Mechanisms linking hypertriglyceridemia to acute pancreatitis

Mechanisms linking hypertriglyceridemia to acute pancreatitis

Hypertriglyceridemia and acute pancreatitis: clinical and basic research—a narrative review

Activation of AMPK Ameliorates Acute Severe Pancreatitis by Suppressing Pancreatic Acinar Cell Necroptosis in Obese Mice Models

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