Efficacy of a yeast postbiotic on cold/flu symptoms in healthy children: A randomized-controlled trial.

BACKGROUND: Children attending school/daycare are at high risk of acute respiratory tract infections. EpiCorTM postbiotic, derived from yeast fermentate, has been demonstrated to improve immune function in adults, reducing the incidence of cold/flu-like or allergy symptoms. As such, studies are warranted in children as available pharmaceutical options have unwanted side effects. METHODS: Two-hundred and fifty-six children aged 4-12 years attending school/daycare were randomized to either EpiCor or Placebo for 84 days during the 2022-2023 flu season in Ontario, Canada. The Canadian Acute Respiratory Illness and Flu Scale (CARIFS) and study diary assessed the incidence and severity of cold/flu symptoms and the use of cold/flu medications. Adverse events were recorded. RESULTS: Total CARIFS severity scores, 'sore throat' and 'muscle aches or pains' symptom scores in the EpiCor group were significantly lower compared to Placebo during incidences of cold/flu (P ≤ 0.05). Participants taking Placebo were 1.73 times more likely to use cold/flu medication compared to those receiving EpiCor (P = 0.04). The incidence of cold/flu symptoms was not significantly different between groups. EpiCor was found to be safe and well-tolerated. CONCLUSIONS: EpiCor supplementation resulted in significantly lower cold/flu symptom severity and less cold/flu medication usage than Placebo demonstrating a beneficial effect on immune function in children. IMPACT: Children are at high risk of acquiring cold/flu infections and safe and efficacious mitigating regimens are lacking. Children supplemented daily with 500 mg EpiCorTM postbiotic derived from yeast fermentate had significantly lower overall cold/flu symptom severity, and severity of sore throat and muscle aches or pains over the 84-day supplementation period. EpiCor supplementation resulted in decreased use of traditional cold/flu medication. Daily supplementation with 500 mg of EpiCor for 84 days was safe and well tolerated by healthy children aged 4-12 years attending school or daycare.

Association between Intrapancreatic Fat Deposition and the Leptin/Ghrelin Ratio in the Fasted and Postprandial States.

BACKGROUND: The clinical relevance of excess intrapancreatic fat deposition (IPFD) is increasingly appreciated. Leptin and ghrelin are key players in the regulation of food intake, energy balance, and body fat mass. The aim was to investigate the associations of the leptin/ghrelin ratio and its components with IPFD. METHODS: All participants underwent magnetic resonance imaging on a 3T scanner to quantify IPFD. Both fasting and postprandial blood samples were analyzed for leptin and acylated ghrelin. Linear regression analysis was conducted, accounting for visceral/subcutaneous fat volume ratio, glycated hemoglobin, and other covariates. RESULTS: A total of 94 participants (32 women) with a median age of 56 (interquartile range 44-66) years were studied. Their median IPFD was 9.6% (interquartile range 8.8-10.4%). In the fasted state, the leptin/ghrelin ratio (ß = 0.354; 95% confidence interval 0.044-0.663; p = 0.025, in the most adjusted model) and leptin (ß = 0.040; 95% confidence interval 1.003-1.078; p = 0.035, in the most adjusted model) were significantly associated with IPFD. Ghrelin in the fasted state was not significantly associated with IPFD. In the postprandial state, the leptin/ghrelin ratio, leptin, and ghrelin were not significantly associated with IPFD. CONCLUSION: Fasting circulating levels of leptin are directly associated with IPFD. Purposely designed mechanistic studies are warranted to determine how high leptin may contribute to excess IPFD.

Implications of Tobacco Smoking and Alcohol Consumption on Ectopic Fat Deposition in Individuals After Pancreatitis.

OBJECTIVES: Tobacco smoking and alcohol consumption are established risk factors for pancreatitis. This study investigated the associations between tobacco smoking/alcohol consumption in people after an attack of pancreatitis and intrapancreatic fat deposition (IPFD), intrahepatic fat deposition (IHFD), and skeletal muscle (SMFD) fat deposition. METHODS: In this cross-sectional study, magnetic resonance imaging was used to quantify IPFD, IHFD, and SMFD by 2 independent raters. A validated questionnaire was used to determine tobacco smoking and alcohol consumption. RESULTS: A total of 119 individuals after an attack of pancreatitis were included. Average tobacco smoking contributed most to variance in IPFD (R = 6.5%) and least to variance in SMFD (R = 0.4%). Average alcohol consumption contributed most to variance in variance in IPFD (R = 2.8%) and least to IHFD (R = 1.1%). Packs/day contributed more than years of smoking to variance in IPFD (R = 4.9 and 0.2%, correspondingly), whereas years of drinking contributed more than average daily alcohol consumption (R = 3.9 and 3.2%, correspondingly). CONCLUSIONS: Tobacco smoking and alcohol consumption contributed more to variance in IPFD than IHFD and SMFD. Smoking contributed more than drinking to variance in IPFD. The daily amount of tobacco smoked appeared to be more important than years of smoking for IPFD.

Psoas muscle size as a magnetic resonance imaging biomarker of progression of pancreatitis.

OBJECTIVE: Pancreatitis often represents a continuous inflammatory process, from the first episode of acute pancreatitis (FAP) to recurrent acute pancreatitis (RAP) to chronic pancreatitis (CP). Psoas muscle size is a validated surrogate for global skeletal mass, changes in which are associated with inflammation. The objective was to investigate psoas muscle size in individuals following FAP, RAP, and CP, as well as its associations with pro-inflammatory cytokines. METHODS: Individuals following pancreatitis and healthy individuals were recruited. All participants underwent magnetic resonance imaging, from which psoas muscle volume was derived independently by two raters in a blinded fashion. Circulating levels of four major cytokines (interleukin-6, tumour necrosis factor-α, C-C motif chemokine ligand 2, and leptin) were measured. Five linear regression additive models were built to adjust for possible confounders (age, sex, body composition, physical activity, tobacco smoking, alcohol consumption, comorbidities, and endocrine and exocrine pancreatic functions). RESULTS: A total of 145 participants were enrolled. A significant downward trend in psoas muscle volume was observed between healthy controls and individuals following FAP, RAP, and CP in all adjusted models (p = 0.047, 0.005, 0.004, and < 0.001). Leptin was significantly associated with psoas muscle volume in all models (ß = - 0.16, p = 0.030 in the most adjusted model). The other studied cytokines were not significantly associated with psoas muscle volume. CONCLUSIONS: Psoas muscle size is significantly reduced along the continuum from FAP to RAP to CP. Leptin appears to be one of the factors implicated in this. Further studies are warranted to investigate the relationship between skeletal muscle and inflammation of the pancreas. KEY POINTS: • First acute pancreatitis, recurrent acute pancreatitis, and chronic pancreatitis were associated with progressively reduced psoas muscle size. • The findings were independent of age, sex, body fat composition, physical activity, tobacco smoking, alcohol consumption, comorbidities, and exocrine and endocrine functions of the pancreas. • The mechanism underlying the observed findings may involve hyperleptinaemia.

Elevated Circulating Levels of Motilin are Associated with Diabetes in Individuals after Acute Pancreatitis.

AIM: The study aimed to investigate the associations between glycaemic control after acute pancreatitis and gastrointestinal motility, using plasma motilin concentration and gastroparesis cardinal symptom index score as proxies. METHODS: This cross-sectional study recruited a total of 93 individuals after acute pancreatitis. Gastroparesis cardinal index scores, demographic and anthropometric factors, as well as pancreatitis-related factors were analysed. Fasting venous blood was collected to measure motilin, glycated haemoglobin, and fasting blood glucose. Linear regression analyses were conducted to investigate the associations between glycaemic control and gastrointestinal motility in unadjusted and adjusted models. RESULTS: Motilin was significantly higher in individuals with diabetes across all adjusted models, with the highest ß-coefficient (95% confidence interval) of 588.89 (138.50, 1039.28); P=0.010. Fasting blood glucose was significantly associated with motilin across all models, with the highest ß-coefficient (95% confidence interval) of 156.30 (55.49, 257.10); P=0.002. Glycated haemoglobin was significantly associated with motilin in one adjusted model with ß-coefficient (95% confidence interval) of 18.78 (1.53, 36.02); P=0.033. Gastroparesis cardinal symptom index was not significantly associated with any measure of glycaemic control. CONCLUSIONS: Diabetes in individuals after acute pancreatitis appears to be characterised by elevated plasma motilin but not gastroparesis cardinal symptom index. The role of motilin in this setting warrants further investigations.

Associations between ketone bodies and fasting plasma glucose in individuals with post-pancreatitis prediabetes.

Context: Levels of ketone bodies are altered in both acute pancreatitis and type 1 and type 2 diabetes. However, the role of ketone bodies in the pathogenesis of abnormal glucose metabolism after pancreatitis is largely unknown.Objective: To investigate the associations between ketone bodies and glucose homeostasis in individuals with post-pancreatitis prediabetes (PPP) versus normoglycaemia after pancreatitis (NAP).Methods: Fasting blood samples were analysed for acetoacetate, ß-hydroxybutyrate, and markers of glucose metabolism at a median of 26 months after acute pancreatitis. A series of linear regression analyses were conducted adjusting for patient- and pancreatitis-related characteristics.Results: The study included 27 individuals with PPP and 52 with NAP. ß-hydroxybutyrate was significantly associated with fasting plasma glucose (p = .002) and explained 26.2% of its variance in PPP, but not in NAP (p = .814; 0%). Acetoacetate was not significantly associated with fasting plasma glucose in both PPP (p = .681) or NAP (p = .661).Conclusions: An inverse association between ß-hydroxybutyrate and fasting plasma glucose characterises PPP and this may have translational implications.

Pancreatic Hormone Responses to Mixed Meal Test in New-onset Prediabetes/Diabetes After Non-necrotizing Acute Pancreatitis.

AIM: To investigate the pancreatic hormone responses to mixed meal test, in particular changes in insulin secretion, insulin sensitivity, and their interrelationship, in individuals with new-onset prediabetes or diabetes after non-necrotizing acute pancreatitis (NODAP) compared with healthy controls. METHODS: Twenty-nine individuals with NODAP and 29 age-and sex-matched healthy controls were recruited. All participants (after fasting for at least 8 h) were given 12 oz. of BOOST drink and blood samples were collected before and after stimulation to measure insulin, C-peptide, glucagon, and pancreatic polypeptide. Indices of insulin sensitivity (HOMA-IS, 1/fasting insulin, Raynaud, and Matsuda) and insulin secretion (HOMA-ß, Stumvoll, insulinogenic index 30' and 60') were calculated. Repeated measures analyses were conducted in the unadjusted and adjusted models. RESULTS: Insulin and C-peptide levels were significantly higher in individuals with NODAP compared with controls during mixed meal test in both the unadjusted (P=0.001 for both) and adjusted (P=0.004 and P=0.006, respectively) models. HOMA-IS (P=0.005), 1/fasting insulin (P=0.018), Raynaud index (P=0.018), and Matsuda index (P=0.021) were significantly lower in individuals with NODAP, whereas HOMA-ß (P=0.028) and Stumvoll index (P=0.013) were significantly higher. Glucagon and pancreatic polypeptide levels did not differ significantly between NODAP and controls during mixed meal test in both the unadjusted (P=0.345 and P=0.206, respectively) and adjusted (P=0.359 and P=0.158, respectively) models. CONCLUSIONS: Decreased insulin sensitivity, ß-cell compensation, and no significant change in postprandial levels of glucagon and pancreatic polypeptide characterize NODAP. The above findings may help develop an evidence-based protocol with a view to optimize control of glucose homeostasis in NODAP.

Relationship of pancreas volume to tobacco smoking and alcohol consumption following pancreatitis.

BACKGROUND: Tobacco smoking and alcohol consumption are established risk factors for diseases of the pancreas. With the recent advances in imaging modalities (such as magnetic resonance (MR) imaging), opportunities have arisen to study pancreas size, in both health and disease. Studies investigating the relationship between tobacco smoking, alcohol consumption, and total pancreas volume (TPV) - a holistic measure of pancreatic exocrine reserve - are lacking. The aim of the present study was to investigate the associations between MR-derived TPV and tobacco smoking/alcohol consumption. METHODS: This cross-sectional study recruited individuals with a history of pancreatitis and healthy controls. A validated questionnaire was used to ascertain current and lifetime tobacco smoking and alcohol consumption. TPV was quantified using MR images by two independent raters. Generalized additive models and linear regression analyses were conducted and adjusted for demographic, metabolic, and pancreatitis-related factors. RESULTS: A total of 107 individuals following pancreatitis and 38 healthy controls were included. There was no statistically significant difference in TPV between any of the tobacco smoking/alcohol consumption categories of individuals following pancreatitis and healthy controls, in both unadjusted and adjusted analyses. In individuals following pancreatitis, multivariate linear regression found no association between TPV and 7 smoking- and alcohol-related variables. Sensitivity analyses constrained to individuals who did not abstain from either smoking or drinking following their first attack of pancreatitis did not yield statistical significance with TPV. In post-hoc analysis, age was significantly inversely associated with TPV in the most adjusted model (p = 0.016). CONCLUSIONS: This is the first study to investigate the association between tobacco smoking, alcohol consumption, and MR-derived TPV following pancreatitis. It appears that age, but not tobacco smoking or alcohol consumption, is associated with a significantly reduced TPV.

Circulating levels of lipocalin-2 are associated with fatty pancreas but not fatty liver.

Lipocalin-2 (LCN-2), a peptide with diverse expression pattern, has been identified as a biomarker of various diseases as well as a factor contributing to inflammatory responses associated with excess adiposity and ensuing metabolic disorders. Although the inter-relationship between LCN-2 and excess adiposity is increasingly recognized, little is known about the inter-relationship between LCN-2 and ectopic fat deposition. The present study aimed to investigate the associations between LCN-2 and fatty pancreas as well as fatty liver. In addition, the associations between LCN-2 and pro-inflammatory cytokines were studied. Magnetic resonance imaging was used to quantify intra-pancreatic fat deposition and visceral-to-subcutaneous fat volume ratio whereas magnetic resonance spectroscopy was used to quantify liver fat deposition. Fasting venous blood was analyzed for LCN-2, C-C motif chemokine ligand 2, interleukin-6, leptin, tumor necrosis factor-α, glycated hemoglobin, glucose, and insulin. Binary logistic regression and linear regression analyses were conducted. Three statistical models were built to adjust for demographics, comorbidities, levels of glycated hemoglobin, insulin resistance, and abdominal fat distribution. A total of 79 individuals were studied, of whom 20 had fatty pancreas, 14 had fatty liver, and 4 had both. Lipocalin-2 was significantly associated with fatty pancreas in all the adjusted models (p = 0.014 in the most adjusted model) but was not significantly associated with fatty liver in any of the studied models. Lipocalin-2 was significantly associated with interleukin-6 and tumor necrosis factor-α, in both the unadjusted and adjusted models. Leptin and C-C motif chemokine ligand 2 were not significantly associated with LCN-2 in any of the studied models. These findings suggest that LCN-2 is a potential biomarker of fatty pancreas, independent of abdominal fat distribution, insulin resistance, and other covariates. The role of LCN-2 in intra-pancreatic fat deposition and related low-grade inflammation warrants further investigations.

Serum lipid profile as a biomarker of intra-pancreatic fat deposition: A nested cross-sectional study.

BACKGROUND AND AIMS: The relationship between intra-pancreatic fat deposition (IPFD) and lipid profile has been investigated in individuals with obesity and/or type 2 diabetes, but not in healthy non-obese individuals and those after acute pancreatitis. The aim of the study was to investigate the association between serum lipid profile and IPFD in the latter individuals and to determine the effect of abdominal fat distribution and other covariates. METHODS AND RESULTS: A total of 90 individuals with a history of acute pancreatitis as well as 23 healthy non-obese individuals participated in the study. Magnetic resonance imaging was used to quantify IPFD and visceral-to-subcutaneous fat volume ratio, followed by fasting state measurement of high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), TC/HDL-C ratio, and triglycerides. In healthy non-obese individuals, IPFD was not significantly associated with any of the studied markers. In individuals after acute pancreatitis, IPFD was significantly associated with triglycerides in both unadjusted (ß = 0.360; 95% CI, 0.090-0.629; p = 0.009) and adjusted models, with a ß-coefficient of 0.280 [(95% CI, 0.016-0.545); p = 0.038] in the most adjusted model. Also, IPFD was significantly associated with TC/HDL-C ratio in both unadjusted (ß = 0.336; 95% CI, 0.045-0.626; p = 0.024) and adjusted models, with a ß-coefficient of 0.375 [(95% CI, 0.090-0.660); p = 0.010] in the most adjusted model. Multiple regression yielded triglycerides, but not TC/HDL-C ratio, as a significant marker of IPFD in individuals after acute pancreatitis. CONCLUSIONS: Serum lipid profile is not associated with IPFD in healthy non-obese. Triglycerides, but not other components of lipid profile, is a promising biomarker for IPFD in individuals following acute pancreatitis.

Glucose Counter-regulation After Acute Pancreatitis.

OBJECTIVES: Persistent hyperglycemia is a common sequela of acute pancreatitis (AP). The role of counter-regulatory hormones in maintaining glucose homeostasis has been largely studied during the course of AP, but not after clinical resolution of the disease. The objectives of this study were to investigate the associations between circulating levels of glucagon, cortisol, and human growth hormone and glucose homeostasis after AP as well as their associations with a comprehensive panel of pancreatic hormones, gut peptides, and proinflammatory cytokines. METHODS: Participants with no history of pre-existing prediabetes or diabetes were categorized into hyperglycemia and normoglycemia after AP groups. Binary logistic regression and linear regression analyses were conducted. RESULTS: Eighty-three individuals were included, of whom 19 had hyperglycemia. Glucagon, cortisol, and human growth hormone did not differ significantly between the groups. Glucagon explained up to 86% of the variance in glucagon-like peptide 1, whereas cortisol explained up to 89% of the variance in interleukin 6 in hyperglycemia after AP. CONCLUSIONS: Counter-regulatory hormones do not appear to play a direct role in the mechanisms underlying hyperglycemia after AP. However, significant associations between glucagon and glucagon-like peptide 1, as well as between cortisol and interleukin 6, suggest that that these hormones may be involved indirectly in the pathophysiology of hyperglycemia after AP.

Associations between intra-pancreatic fat deposition and circulating levels of cytokines.

While a plethora of studies have been conducted to investigate the associations between pro-inflammatory cytokines and obesity, the inter-relationship between pro-inflammatory cytokines and intra-pancreatic fat deposition (IPFD) has been poorly investigated. In the present study, circulating levels of C-C motif chemokine ligand 2 (CCL2), interleukin-6 (IL-6), leptin, and tumor necrosis factor-alpha (TNFα) were measured in 90 individuals after acute pancreatitis (AP) as well as 21 healthy non-obese individuals. Magnetic resonance imaging was used to quantify IPFD and visceral-to-subcutaneous fat volume ratio by two independent raters. Linear regression analyses were performed to investigate the associations between IPFD and each cytokine, adjusting for demographic, metabolic, and pancreatitis-related factors, as well as abdominal fat distribution. In healthy non-obese individuals, IPFD was not significantly associated with any of the studied cytokines in both the unadjusted and adjusted models. In individuals after AP, IPFD was significantly associated with leptin in the models adjusted for age and sex (ß = 0.063 [95% confidence interval: 0.007, 0.119], P = 0.026); age, sex, visceral-to-subcutaneous fat volume ratio, glycated hemoglobin, and pancreatitis-related factors (ß = 0.056 [95% confidence interval: 0.000, 0.111], P = 0.049). Also, IPFD was significantly associated with TNFα in the unadjusted model (ß = 0.102 [95% confidence interval: 0.002, 0.202], P = 0.045) and the model adjusted for age, sex, visceral-to-subcutaneous fat volume ratio, glycated hemoglobin, and pancreatitis-related factors (ß = 0.128 [95% confidence interval: 0.034, 0.223], P = 0.008). The associations between IPFD and IL-6, CCL2 were not statistically significant, in both the unadjusted and adjusted models. These findings indicate that leptin and TNFα are associated with IPFD independent of abdominal fat distribution and other covariates in individuals after AP. The role of IPFD in low-grade inflammation warrants further investigations.

Relationship of Anthropometric Indices to Abdominal Body Composition: A Multi-Ethnic New Zealand Magnetic Resonance Imaging Study.

BACKGROUND: Conventional anthropometric indices (body mass index (BMI) and waist circumference (WC)) have limitations, in part, due to ethnic differences in fat distribution. Assessment of abdominal body composition using magnetic resonance imaging (MRI) is increasingly used to gain deeper insights into the pathophysiology of diabetes mellitus, cardiovascular diseases and metabolic syndrome, but the knowledge of abdominal volumes in indigenous populations is scarce. This study aimed to assess abdominal fat distribution and total abdominal volume using MRI in a multi-ethnic cohort that includes Maori (the indigenous people of New Zealand) and Pacific Islanders (PI). METHODS: MRI was used to quantify subcutaneous adipose tissue (SAT) volume, visceral adipose tissue (VAT) volume and total abdominal (TAb) volume by two independent raters in a blinded fashion. WC and BMI were also measured. Multinomial regression was used to compare the volumes between ethnic groups. Linear regression was used to investigate the ethnicity-specific associations between anthropometric indices and abdominal volumes. Three statistical models were built to adjust for age, sex, prediabetes/diabetes status and other covariates. RESULTS: A total of 87 individuals (37 Caucasians, 24 Maori/PI and 26 others) were studied. Maori/PI had a significantly higher VAT volume compared with Caucasians across all statistical models, with the highest odds ratio of 2.1 (95% confidence interval: 1.1 - 4.2; P = 0.026). SAT and TAb volumes did not differ significantly between the groups. WC explained up to 72.9% of variance in VAT volume among Maori/PI and up to 50.7% among Caucasians. BMI explained up to 67.6% of variance in VAT volume among Maori/PI and up to 52.1% among Caucasians. CONCLUSIONS: Greater visceral fat deposition among Maori/PI might go some way towards explaining the increased rates of metabolic disorders observed in this ethnic group. Conventional anthropometric indices do not correspond to the same abdominal volumes across different ethnic groups.

Pancreas shrinkage following recurrent acute pancreatitis: an MRI study.

OBJECTIVE: Transition from the first attack of acute pancreatitis (AP) to chronic pancreatitis (CP) via recurrent AP is common. Total pancreas volume (TPV) and pancreas diameters are often reduced in advanced CP but have never been studied after AP. The objective of this study was to investigate pancreas size after clinical resolution of AP and its association with the number of AP attacks. METHODS: Individuals with a history of AP were grouped based on the number of attacks (1, 2, ≥ 3 attacks). Healthy individuals were also recruited. All participants underwent magnetic resonance imaging, from which TPV and pancreas diameters (across the head, body, and tail) were measured independently by two raters in a blinded fashion. Generalised additive models (including age, sex, body mass index, and glycated haemoglobin levels) were used. RESULTS: A total of 123 participants were studied. Total pancreas volume and tail diameter were significantly reduced in both unadjusted (TPV (p = 0.036), tail diameter (p = 0.009)) and adjusted (TPV (p = 0.026), tail diameter (p = 0.034)) models in individuals with ≥ 3 attacks, but not with 1 or 2 attacks, compared with healthy individuals. Head and body diameters did not differ significantly. CONCLUSIONS: Reduced TPV and tail diameter characterise individuals after ≥ 3 attacks of AP and may represent one of the earliest irreversible morphological changes in individuals after AP. A high-risk population for transition to CP might include individuals with at least 3 attacks of AP whereas those with less than 3 attacks might be at a low risk. KEY POINTS: • A significant reduction in total pancreas volume was demonstrated in individuals after 3 or more attacks of acute pancreatitis (without conventional signs of chronic pancreatitis). • Pancreas tail diameter, but not head or body diameter, was reduced in individuals after 3 or more attacks of acute pancreatitis (without conventional signs of chronic pancreatitis). • The above findings were independent of age, sex, body mass index, and glycated haemoglobin levels.

Intrapancreatic fat deposition and visceral fat volume are associated with the presence of diabetes after acute pancreatitis.

Ectopic fat and abdominal adiposity phenotypes have never been studied holistically in individuals after acute pancreatitis (AP). The aim of the study was to investigate phenotypical differences in ectopic fat and abdominal fat between individuals after AP (with and without diabetes) and to determine the role of pancreatitis-related factors. Eighty-four individuals were studied cross-sectionally after a median of 21.5 mo since last episode of AP and were categorized into "diabetes" and "no diabetes" groups. Twenty-eight healthy volunteers were also recruited. With the use of magnetic resonance imaging, intrapancreatic fat percentage, liver fat percentage, visceral fat volume (VFV), subcutaneous fat volume, and visceral-to-subcutaneous (V/S) fat volume ratio were quantified. Analysis of variance was used to investigate the differences in these phenotypes between the groups. All analyses were adjusted for age and sex. Linear regression analysis was used to investigate the association between pancreatitis-related factors and the studied phenotypes. Intrapancreatic fat percentage was significantly higher in the diabetes group (10.2 ± 1.2%) compared with the no diabetes (9.2 ± 1.7%) and healthy volunteers (7.9 ± 1.9%) groups (P < 0.001). VFV was significantly higher in the diabetes (2,715.3 ±1,077.6 cm3) compared with no diabetes (1,983.2 ± 1,092.4 cm3) and healthy volunteer (1,126.2 ± 740.4 cm3) groups (P < 0.001). V/S fat volume ratio was significantly higher in the diabetes (0.97 ± 0.27) compared with no diabetes (0.68 ± 0.42) and healthy volunteer (0.52 ± 0.34) groups (P = 0.001). Biliary AP was associated with significantly higher intrapancreatic fat percentage (ß = 0.67; 95% CI, 0.01, 1.33; P = 0.047). C-reactive protein levels during hospitalization for AP were associated with significantly higher VFV (ß = 3.32; 95% CI, 1.68, 4.96; P < 0.001). In conclusion, individuals with diabetes after AP have higher intrapancreatic fat percentage, VFV, and V/S fat volume ratio. Levels of C-reactive protein during AP are significantly associated with VFV, whereas biliary AP is significantly associated with intrapancreatic fat percentage. NEW & NOTEWORTHY Individuals with diabetes after acute pancreatitis have significantly higher intrapancreatic fat percentage and visceral fat volume compared with individuals without diabetes after acute pancreatitis and healthy controls. C-reactive protein levels during hospitalization for acute pancreatitis and biliary etiology of acute pancreatitis are associated with significantly larger visceral fat and pancreatic fat depots, respectively.

Comprehensive analysis of body composition and insulin traits associated with intra-pancreatic fat deposition in healthy individuals and people with new-onset prediabetes/diabetes after acute pancreatitis.

Current knowledge of biomarkers of intra-pancreatic fat deposition (IFD) is limited. We aimed to analyse comprehensively body composition and insulin traits as biomarkers of IFD in healthy normoglycaemic individuals as well as in individuals with new-onset prediabetes or diabetes after acute pancreatitis (NODAP). A total of 29 healthy individuals and 34 individuals with NODAP took part in this cross-sectional study. The studied biomarkers belonged to the following domains: body composition (anthropometric and MRI-derived variables); indices of insulin secretion; indices of insulin sensitivity; incretins and related peptides; and pancreatitis-related factors. All MRI-derived variables (including IFD) were measured using ImageJ software. Univariate and step-wise regression analyses were conducted to determine variables that best explained variance in IFD. Visceral fat volume and oxyntomodulin were the best biomarkers of IFD in normoglycaemic healthy individuals, contributing to 64% variance. The Raynaud index was the best biomarker of IFD in individuals with NODAP, contributing to 20% variance. Longitudinal studies are warranted to investigate the cause and effect relationship between oxyntomodulin and IFD in healthy individuals, as well as insulin sensitivity and IFD in individuals with NODAP.

Associations between gastrointestinal humoral factors and pancreatic proteolytic enzymes in alcohol-related versus non-alcohol-related pancreatitis.

BACKGROUND: Alcohol-related pancreatitis is common and the gastrointestinal tract plays an important role in the regulation of pancreatic exocrine function. While the relationship between pancreatic proteolytic enzymes and insulin (as well as other pancreatic hormones) has been investigated in detail, little is known about the relationship between pancreatic proteolytic enzymes and gastrointestinal humoral factors. The aim of this study was to study the associations between trypsin, chymotrypsin, and a panel of gastrointestinal humoral factors in patients after an episode of alcohol-related versus non-alcohol-related pancreatitis. METHODS: Fasting venous blood samples were analyzed for trypsin, chymotrypsin, cholecystokinin, gastrin, ghrelin, gastrin-related peptide, neuropeptide Y, peptide YY, secretin, and vasoactive intestinal peptide. Linear regression analysis was used in three statistical models, adjusting for covariates (age, sex, ethnicity, smoking, exercise, body mass index, dysglycemia, recurrence of pancreatitis, duration of pancreatitis, and severity of pancreatitis). RESULTS: The study included 21 patients with alcohol-related pancreatitis and 72 with non-alcohol-related pancreatitis. Gastrin, cholecystokinin, and vasoactive intestinal peptide were significantly associated with chymotrypsin in all three statistical models and resulted in a 1.06, 1.98, and 2.74 times higher chymotrypsin level in alcohol-related pancreatitis, respectively. Ghrelin was significantly associated with trypsin in all three statistical models and resulted in a 2.64 times higher trypsin level in alcohol-related pancreatitis. Other associations did not demonstrate a consistent significant pattern. CONCLUSION: In alcohol-related pancreatitis, several gut-related peptides are significantly associated with pancreatic exocrine function. Further studies to investigate the effect of alcohol on the interaction between cholecystokinin (as well as gastrin, ghrelin, and vasoactive intestinal peptide) and pancreatic exocrine function are warranted.

Gut Hormone Responses to Mixed Meal Test in New-Onset Prediabetes/Diabetes After Acute Pancreatitis.

The study was aimed to investigate gut hormone responses to mixed meal test in individuals with new-onset prediabetes or diabetes after acute pancreatitis (cases) compared with healthy controls, and the effect of body fat parameters. A total of 29 cases and 29 age- and sex-matched healthy controls were recruited. All participants were given standard mixed meal drink and blood samples were collected to measure dipeptidyl peptidase IV, gastric inhibitory peptide, glucagon like peptide-1, insulin, oxyntomodulin, and peptide YY. Body fat parameters were measured using magnetic resonance imaging. Repeated measures and linear regression analyses were conducted in unadjusted and adjusted models. Gastric inhibitory peptide levels were significantly higher whereas oxyntomodulin levels were significantly lower in cases compared with controls in both the unadjusted (p<0.001 and p<0.001, respectively) and adjusted (p<0.001 and p<0.001, respectively) models. In cases, liver fat % contributed up to 13.4% (vs. 2.9% in controls) to variance in circulating levels of gastric inhibitory peptide whereas body mass index - up to 20.8% (vs. 9.9% in controls) in circulating levels of oxyntomodulin. New-onset prediabetes/diabetes after acute pancreatitis is characterised by increased levels of gastric inhibitory peptide and decreased levels of oxyntomodulin. Further, liver fat % and body mass index appear to be the body fat parameters that contribute most significantly to gastric inhibitory peptide and oxyntomodulin levels, respectively.

Profile of Gut Hormones, Pancreatic Hormones and Pro-inflammatory Cytokines in New Zealand Maori.

BACKGROUND: Maori, indigenous people of New Zealand, have at least two times higher prevalence of obesity and diabetes in comparison with the general population in the country. Gut and pancreatic hormone profile differences as well as pro-inflammatory milieu may contribute to this disparity. The aim was to investigate the differences in gut hormones, pancreatic hormones and pro-inflammatory cytokines between Maori and non-Maori individuals. METHODS: This was a cross-sectional study. Fasting blood samples were collected to measure cholecystokinin, ghrelin, gastric inhibitory peptide, glicentin, glucagon-like peptide-1 and -2, oxyntomodulin, secretin, amylin, C-peptide, glucagon, insulin, pancreatic polypeptide, somatostatin, interleukin-6, monocyte chemoattractant protein-1 and tumour necrosis factor-α. Binary logistic regression analysis was conducted in one unadjusted and four adjusted statistical models adjusting for patient-, metabolic- and pancreatitis-related factors. RESULTS: A total of 8 Maori and 85 non-Maori individuals were included. Circulating levels of ghrelin, pancreatic polypeptide and interleukin-6 levels were significantly higher in Maori (P = 0.005, P = 0.003 and P = 0.011, respectively) in both unadjusted and all the four adjusted analyses. Other signaling molecules did not show consistently significant associations with ethnicity. CONCLUSION: Profile of gut hormones, pancreatic hormones and pro-inflammatory cytokines appears to differ between Maori and non-Maori individuals, independent of obesity, diabetes and other covariates. This may go some way to explain the increased propensity to obesity and diabetes in the Maori population.

Pancreas volume in health and disease: a systematic review and meta-analysis.

INTRODUCTION: The pancreas plays a central role in metabolism and is involved in the pathogenesis of several diseases. Pancreas volume is a holistic quantitative measure of pancreas size but the clinical relevance of pancreas volumetry is poorly understood. Areas covered: The aim was to systematically review studies in adults that used computed tomography or magnetic resonance imaging to measure pancreas volume in health and disease, to determine normal pancreas volume range, and to quantify changes in pancreas volume that are associated with disease. Expert commentary: The normal pancreas volume range in adults is 71-83 cm3, with no statistically significant difference between men and women. Type 2 diabetes and type 1 diabetes are associated with a progressively reduced pancreas volume. Overweight and obesity are associated with a progressively increased pancreas volume. There is a paucity of studies on pancreas volume in the setting of diseases of the exocrine pancreas, which should become a research priority in the future.