Effect of Frey's procedure on islet cell function in patients with chronic calcific pancreatitis

Kumar, Ramesh; Sahoo, Jaya Prakash; Pottakat, Biju; Kamalanathan, Sadishkumar; Mohan, Pazhanivel; Kate, Vikram; Kar, Sitanshu Sekhar; Selviambigapathy, Jayakumar

doi:10.1016/j.hbpd.2018.06.001

Cited by 7 publications

(11 citation statements)

References 35 publications

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“…However, in North Indian TCP patients with mild dysglycemia, decreased beta-cell function was noted to be the major factor[ 22 ]. In our study[ 14 ], beta-cell function, as measured by insulin secretion sensitivity index-2 (another composite measure of insulin secretion) was lower in a group of CCP patients with DM compared to CCP patients with prediabetes or normal glucose tolerance (NGT).…”

Section: Beta-cell Dysfunction In Cpmentioning

confidence: 97%

“…Absence of the glucagon response following hypoglycemia was also shown by Larsen et al[ 13 ]. We previously demonstrated that glucagon was not suppressed following an oral glucose load in patients with chronic calcific pancreatitis (CCP) irrespective of their diabetes status[ 14 ]. This suggests that the ability of alpha cells to suppress glucagon secretion in response to glucose is significantly impaired in CCP patients.…”

Section: Alpha Cell Dysfunction In Cpmentioning

confidence: 99%

“…As already described, early dysfunction in insulin secretion and glucagon suppression is seen in CP patients without diabetes[ 11 ]. Indeed, it has been shown that beta cell function and insulin secretion is lower in CP patients with DM compared to CP patients with NGT[ 14 , 38 ]. CP patients with prediabetes are intermediate in terms of beta cell secretary function[ 14 , 38 ].…”

Section: Difference In Islet Cell Function Between Cp With Dm mentioning

confidence: 99%

“…Indeed, it has been shown that beta cell function and insulin secretion is lower in CP patients with DM compared to CP patients with NGT[ 14 , 38 ]. CP patients with prediabetes are intermediate in terms of beta cell secretary function[ 14 , 38 ]. Although our study[ 14 ] showed no difference in glucagon suppression between CP subjects with NGT, prediabetes and diabetes groups at baseline, Knop et al[ 38 ] clearly demonstrated a rise in glucagon level in a continuous manner across NGT to diabetes in CP.…”

Section: Difference In Islet Cell Function Between Cp With Dm mentioning

confidence: 99%

“…CP patients with prediabetes are intermediate in terms of beta cell secretary function[ 14 , 38 ]. Although our study[ 14 ] showed no difference in glucagon suppression between CP subjects with NGT, prediabetes and diabetes groups at baseline, Knop et al[ 38 ] clearly demonstrated a rise in glucagon level in a continuous manner across NGT to diabetes in CP. Moreover, CP patients with DM have significantly low GIP stimulated late insulin secretion (20-120 min) compared to CP with NGT who had a significantly greater insulin response to GIP.…”

Section: Difference In Islet Cell Function Between Cp With Dm mentioning

confidence: 99%

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Islet cell dysfunction in patients with chronic pancreatitis

Roy

Sahoo

Kamalanathan

et al. 2020

WJD

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Chronic pancreatitis (CP) is characterized by progressive inflammation and fibrosis of the pancreas that eventually leads to pancreatic exocrine and endocrine insufficiency. Diabetes in the background of CP is very difficult to manage due to high glycemic variability and concomitant malabsorption. Progressive beta cell loss leading to insulin deficiency is the cardinal mechanism underlying diabetes development in CP. Alpha cell dysfunction leading to deranged glucagon secretion has been described in different studies using a variety of stimuli in CP. However, the emerging evidence is varied probably because of dependence on the study procedure, the study population as well as on the stage of the disease. The mechanism behind islet cell dysfunction in CP is multifactorial. The intra-islet alpha and beta cell regulation of each other is often lost. Moreover, secretion of the incretin hormones such as glucagon like peptide-1 and glucose-dependent insulinotropic polypeptide is dysregulated. This significantly contributes to islet cell disturbances. Persistent and progressive inflammation with changes in the function of other cells such as islet delta cells and pancreatic polypeptide cells are also implicated in CP. In addition, the different surgical procedures performed in patients with CP and antihyperglycemic drugs used to treat diabetes associated with CP also affect islet cell function. Hence, different factors such as chronic inflammation, dysregulated incretin axis, surgical interventions and anti-diabetic drugs all affect islet cell function in patients with CP. Newer therapies targeting alpha cell function and beta cell regeneration would be useful in the management of pancreatic diabetes in the near future.

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Section: Beta-cell Dysfunction In Cpmentioning

confidence: 97%

Section: Alpha Cell Dysfunction In Cpmentioning

confidence: 99%

Section: Difference In Islet Cell Function Between Cp With Dm mentioning

confidence: 99%

Section: Difference In Islet Cell Function Between Cp With Dm mentioning

confidence: 99%

Section: Difference In Islet Cell Function Between Cp With Dm mentioning

confidence: 99%

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Islet cell dysfunction in patients with chronic pancreatitis

Roy

Sahoo

Kamalanathan

et al. 2020

WJD

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Pancreatic Crosstalk in the Disease Setting: Understanding the Impact of Exocrine Disease on Endocrine Function

Villaca,

Mastracci

2024

Comprehensive Physiology

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The exocrine and endocrine are functionally distinct compartments of the pancreas that have traditionally been studied as separate entities. However, studies of embryonic development, adult physiology, and disease pathogenesis suggest there may be critical communication between exocrine and endocrine cells. In fact, the incidence of the endocrine disease diabetes secondary to exocrine disease/dysfunction ranges from 25% to 80%, depending on the type and severity of the exocrine pathology. Therefore, it is necessary to investigate how exocrine‐endocrine “crosstalk” may impact pancreatic function. In this article, we discuss common exocrine diseases, including cystic fibrosis, acute, hereditary, and chronic pancreatitis, and the impact of these exocrine diseases on endocrine function. Additionally, we review how obesity and fatty pancreas influence exocrine function and the impact on cellular communication between the exocrine and endocrine compartments. Interestingly, in all pathologies, there is evidence that signals from the exocrine disease contribute to endocrine dysfunction and the progression to diabetes. Continued research efforts to identify the mechanisms that underlie the crosstalk between various cell types in the pancreas are critical to understanding normal pancreatic physiology as well as disease states. © 2024 American Physiological Society. Compr Physiol 14:5371‐5387, 2024.

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Different post-pancreatectomy glucagon responses to a meal test between surgical approaches

Matsuda,

Himeno,

Nakashima

et al. 2023

Endocr J

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Residual pancreatic endocrine function is important for maintaining metabolic status after pancreatectomy and is closely related to patient nutritional status and prognosis. In contrast to insulin secretion, the significance of glucagon secretion following pancreatectomy remains unclear. In this study, we assessed the changes in pancreatic glucagon secretion during pancreatectomy to determine their pathophysiological significance. We evaluated glucagon and insulin secretion using a liquid meal tolerance test before and after pancreatectomy in patients scheduled to undergo pancreaticoduodenectomy (PD) or distal pancreatectomy (DP). After pancreatectomy, fasting plasma glucagon levels were significantly decreased in both the PD (n = 10) and DP (n = 5) groups (PD: from 18.4 to 10.5 pg/mL, p = 0.037; DP: from 21.0 to 12.1 pg/mL, p = 0.043), whereas postprandial plasma glucagon levels were not changed. In the liquid meal tolerance test after pancreatectomy, 60-min plasma glucagon levels and the area under the curve (AUC) for 0-120 min of PD were significantly higher than those for DP (60-min plasma glucagon: PD 49.0 vs. DP 21.7 pg/mL, p = 0.040; AUC 0-120min : PD 4,749 vs. DP 3,564 μg min/mL, p = 0.028). Postoperative plasma glucose, serum insulin, and serum C-peptide levels during the liquid meal tolerance test were not significantly different between the two groups. Although fasting plasma glucagon levels decreased, postprandial glucagon responses were maintained after both PD and DP. The difference in residual meal-stimulated glucagon response between PD and DP suggests that a relative excess of postprandial glucagon is involved in the postoperative nutritional status after PD through its impact on systemic metabolic status.

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Effect of Frey's procedure on islet cell function in patients with chronic calcific pancreatitis

Cited by 7 publications

References 35 publications

Islet cell dysfunction in patients with chronic pancreatitis

Islet cell dysfunction in patients with chronic pancreatitis

Pancreatic Crosstalk in the Disease Setting: Understanding the Impact of Exocrine Disease on Endocrine Function

Different post-pancreatectomy glucagon responses to a meal test between surgical approaches

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