The Relationship between Abdominal Fat Phenotypes and Insulin Resistance in Non-Obese Individuals after Acute Pancreatitis

Ko, Jung Hwa; Skudder-Hill, Loren; Cho, Jaelim; Bharmal, Sakina H; Petrov, Maxim S.

doi:10.3390/nu12092883

Cited by 24 publications

(12 citation statements)

References 59 publications

(77 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consistent with this, it has been reported that obesity increases the risk of IR development in patients with AP (58). Furthermore, in non-obese AP patients, increased intra-pancreatic fat deposition was associated with an increased HOMA-IR (homeostasis model assessment-IR) index (59). Among the inflammatory mediators, the adipocytokine IL-6 has been shown to be associated with elevated levels of chronic hyperglycaemia and IR after AP (60).…”

Section: Post-acute Pancreatitis Diabetes Mellitussupporting

confidence: 62%

Mechanisms of Post-Pancreatitis Diabetes Mellitus and Cystic Fibrosis-Related Diabetes: A Review of Preclinical Studies

et al. 2021

View full text Add to dashboard Cite

Anatomical proximity and functional correlations between the exocrine and endocrine pancreas warrant reciprocal effects between the two parts. Inflammatory diseases of the exocrine pancreas, such as acute or chronic pancreatitis, or the presence of cystic fibrosis disrupt endocrine function, resulting in diabetes of the exocrine pancreas. Although novel mechanisms are being increasingly identified, the intra- and intercellular pathways regulating exocrine–endocrine interactions are still not fully understood, making the development of new and more effective therapies difficult. Therefore, this review sought to accumulate current knowledge regarding the pathogenesis of diabetes in acute and chronic pancreatitis, as well as cystic fibrosis.

show abstract

Section: Post-acute Pancreatitis Diabetes Mellitussupporting

confidence: 62%

Mechanisms of Post-Pancreatitis Diabetes Mellitus and Cystic Fibrosis-Related Diabetes: A Review of Preclinical Studies

et al. 2021

View full text Add to dashboard Cite

show abstract

“…AP is very common, has a considerably high mortality rate and can cause systemic complications (3). The mortality rate of AP has increased from 15 to 30% (4), while the combination of AP with sepsis increases the mortality rate to >50% (5). Although significant efforts have been made to prevent and treat AP (6), no specific treatment methods are currently available.…”

Section: Introductionmentioning

confidence: 99%

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Wen

Tang

et al. 2021

Mol Med Rep

View full text Add to dashboard Cite

Acute pancreatitis (AP) is one of the most frequent gastrointestinal diseases and has no specific treatment. It has been shown that dysfunction of pancreatic acinar cells can lead to AP progression. Emodin is a natural product, which can alleviate the symptoms of AP. However, the mechanism by which emodin regulates the function of pancreatic acinar cells remains unclear. Thus, the present study aimed to investigate the mechanism by which emodin modulates the function of pancreatic acinar cells. To mimic AP in vitro, pancreatic acinar cells were cotreated with caerulein and lipopolysaccharide (LPS). Exosomes were isolated using the ExoQuick precipitation kit. Western blot analysis, Nanosight Tracking analysis and transmission electron microscopy were performed to detect the efficiency of exosome separation. Gene expression was detected by reverse transcription-quantitative PCR. The levels of IL-1β and TNF-α were detected by ELISA. The data indicated that emodin significantly decreased the levels of IL-1β and TNF-α in the supernatant samples derived from AR42J cells cotreated with caerulein and LPS. In addition, emodin significantly promoted the proliferation of AR42J cells cotreated with caerulein and LPS, and inhibited apoptosis, while the effect of emodin was reversed by long non-coding (lnc)RNA taurine upregulated 1 (TUG1) overexpression. The expression level of TUG1 in AR42J cells or exosomes derived from AR42J cells was significantly increased following treatment of the cells with LPS and caerulein, while this effect was notably reversed by emodin treatment. In addition, exosomes derived from caerulein and LPS cotreated AR42J cells inhibited the differentiation and anti-inflammatory function of regulatory T cells, while treatment of the cells with emodin significantly decreased this effect. In conclusion, the data indicated that emodin inhibited the induction of inflammation in AR42J cells by regulating the expression of cellular and exosomal lncRNA. Therefore, emodin may be used as a potential agent for the treatment of AP.

show abstract

“…One study showed a significant inverse association between leptin and intra-pancreatic fat deposition (determined with the use of magnetic resonance imaging), independent of abdominal fat distribution in individuals after an attack of acute pancreatitis [65]. Taking into account that individuals after an attack of pancreatitis have significantly higher intra-pancreatic fat deposition compared with healthy controls [66] and given the findings of significant inverse associations of intra-pancreatic fat deposition and indices of insulin sensitivity in non-obese NODAP individuals (but not in T2DM) [67], leptin could be a potential driver of glucose metabolism abnormalities in NODAP. Second, it is thought that leptin may share similar appetite regulating pathways with oxyntomodulin-a gut peptide that whose circulating levels are lower in individuals with NODAP [68].…”

Section: Discussionmentioning

confidence: 99%

Relationship between Energy Balance and Circulating Levels of Hepcidin and Ferritin in the Fasted and Postprandial States

Kimita

Bharmal

et al. 2021

Nutrients

Self Cite

View full text Add to dashboard Cite

Markers of iron metabolism are altered in new-onset diabetes, but their relationship with metabolic signals involved in the maintenance of energy balance is poorly understood. The primary aim was to explore the associations between markers of iron metabolism (hepcidin and ferritin) and markers of energy balance (leptin, ghrelin, and the leptin/ghrelin ratio) in both the fasted and postprandial states. These associations were also studied in the sub-groups stratified by diabetes status. This was a cross-sectional study of individuals without disorders of iron metabolism who were investigated after an overnight fast and, in addition, some of these individuals underwent a mixed meal test to determine postprandial responses of metabolic signals. The associations between hepcidin, ferritin, and leptin, ghrelin, leptin/ghrelin ratio were studied using several multiple linear regression models. A total of 76 individuals in the fasted state and 34 individuals in the postprandial state were included. In the overall cohort, hepcidin was significantly inversely associated with leptin (in the most adjusted model, the β coefficient ± SE was −883.45 ± 400.94; p = 0.031) and the leptin/ghrelin ratio (in the most adjusted model, the β coefficient ± SE was −148.26 ± 61.20; p = 0.018) in the fasted state. The same associations were not statistically significant in the postprandial state. In individuals with new-onset prediabetes or diabetes (but not in those with normoglycaemia or longstanding prediabetes or diabetes), hepcidin was significantly inversely associated with leptin (in the most adjusted model, the β coefficient ± SE was −806.09 ± 395.44; p = 0.050) and the leptin/ghrelin ratio (in the most adjusted model, the β coefficient ± SE was −129.40 ± 59.14; p = 0.037). Leptin appears to be a mediator in the link between iron metabolism and new-onset diabetes mellitus. These findings add to the growing understanding of mechanisms underlying the derangements of glucose metabolism.

show abstract

The Relationship between Abdominal Fat Phenotypes and Insulin Resistance in Non-Obese Individuals after Acute Pancreatitis

Cited by 24 publications

References 59 publications

Mechanisms of Post-Pancreatitis Diabetes Mellitus and Cystic Fibrosis-Related Diabetes: A Review of Preclinical Studies

Mechanisms of Post-Pancreatitis Diabetes Mellitus and Cystic Fibrosis-Related Diabetes: A Review of Preclinical Studies

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Relationship between Energy Balance and Circulating Levels of Hepcidin and Ferritin in the Fasted and Postprandial States

Contact Info

Product

Resources

About