The aim of this study was to test the effect of a plant-based dietary intervention on beta-cell function in overweight adults with no history of diabetes. Participants (n = 75) were randomized to follow a low-fat plant-based diet (n = 38) or to make no diet changes (n = 37) for 16 weeks. At baseline and 16 weeks, beta-cell function was quantified with a mathematical model. Using a standard meal test, insulin secretory rate was calculated by C-peptide deconvolution. The Homeostasis Model Assessment (HOMA-IR) index was used to assess insulin resistance while fasting. A marked increase in meal-stimulated insulin secretion was observed in the intervention group compared with controls (interaction between group and time, Gxt, p < 0.001). HOMA-IR index fell significantly (p < 0.001) in the intervention group (treatment effect -1.0 (95% CI, -1.2 to -0.8); Gxt, p = 0.004). Changes in HOMA-IR correlated positively with changes in body mass index (BMI) and visceral fat volume (r = 0.34; p = 0.009 and r = 0.42; p = 0.001, respectively). The latter remained significant after adjustment for changes in BMI (r = 0.41; p = 0.002). Changes in glucose-induced insulin secretion correlated negatively with BMI changes (r = -0.25; p = 0.04), but not with changes in visceral fat. Beta-cell function and insulin sensitivity were significantly improved through a low-fat plant-based diet in overweight adults.

• Klíčová slova
• beta-cell function, diabetes, diet, nutrition, vegan,
• MeSH
• absorpční fotometrie MeSH
• adipozita MeSH
• beta-buňky metabolismus   MeSH
• dieta s omezením tuků * MeSH
• dieta veganská * MeSH
• dospělí MeSH
• energetický příjem MeSH
• hmotnostní úbytek MeSH
• index tělesné hmotnosti MeSH
• inzulin krev   metabolismus   MeSH
• inzulinová rezistence * MeSH
• lidé středního věku MeSH
• lidé MeSH
• nadváha krev   diagnostické zobrazování   dietoterapie   metabolismus   MeSH
• nitrobřišní tuk diagnostické zobrazování   MeSH
• obezita krev   diagnostické zobrazování   dietoterapie   metabolismus   MeSH
• postprandiální období MeSH
• redukční dieta * MeSH
• sekrece inzulinu MeSH
• senioři MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• randomizované kontrolované studie MeSH
• Geografické názvy
• District of Columbia MeSH
• Názvy látek
• inzulin MeSH

Reduced beta cell mass in pancreatic islets (PI) of Goto-Kakizaki (GK) rats is frequently observed in this diabetic model, but knowledge on delta cells is scarce. Aiming to compare delta cell physiology/pathology of GK to Wistar rats, we found that delta cell number increased over time as did somatostatin mRNA and delta cells distribution in PI is different in GK rats. Subtle changes in 6-week-old GK rats were found. With maturation and aging of GK rats, disturbed cytoarchitecture occurred with irregular beta cells accompanied by delta cell hyperplasia and loss of pancreatic polypeptide (PPY) positivity. Unlike the constant glucose-stimulation index for insulin PI release in Wistar rats, this index declined with GK age, whereas for somatostatin it increased with age. A decrease of GK rat PPY serum levels was found. GK rat body weight decreased with increasing hyperglycemia. Somatostatin analog octreotide completely blocked insulin secretion, impaired proliferation at low autocrine insulin, and decreased PPY secretion and mitochondrial DNA in INS-1E cells. In conclusion, in GK rats PI, significant local delta cell hyperplasia and suspected paracrine effect of somatostatin diminish beta cell viability and contribute to the deterioration of beta cell mass. Altered PPY-secreting cells distribution amends another component of GK PI's pathophysiology.

• MeSH
• antagonisté inzulinu farmakologie   MeSH
• beta-buňky účinky léků   metabolismus   patologie   MeSH
• buňky vylučující somatostatin účinky léků   metabolismus   patologie   MeSH
• diabetes mellitus 2. typu krev   metabolismus   patologie   MeSH
• hyperplazie MeSH
• imunohistochemie MeSH
• inbrední kmeny potkanů MeSH
• inzulin metabolismus   MeSH
• inzulinová rezistence * MeSH
• messenger RNA metabolismus   MeSH
• nádorové buněčné linie MeSH
• oktreotid farmakologie   MeSH
• pankreatický polypeptid antagonisté a inhibitory   genetika   metabolismus   MeSH
• potkani Wistar MeSH
• proliferace buněk účinky léků   MeSH
• sekrece inzulinu MeSH
• somatostatin antagonisté a inhibitory   genetika   metabolismus   MeSH
• stárnutí * MeSH
• viabilita buněk účinky léků   MeSH
• vývojová regulace genové exprese MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antagonisté inzulinu MeSH
• inzulin MeSH
• messenger RNA MeSH
• oktreotid MeSH
• pankreatický polypeptid MeSH
• somatostatin MeSH

BACKGROUND: Abnormal postprandial elevation of plasma glucose and lipids plays an important role in the pathogenesis of diabetes and strongly predicts cardiovascular mortality. In patients suffering from type 2 diabetes (T2D) postprandial state is associated with oxidative stress, cardiovascular risk and, probably, with impairment of both secretion and the effect of gastrointestinal peptides. Evaluating postprandial changes of gastrointestinal hormones together with changes in oxidative stress markers may help to understand the mechanisms behind the postprandial state in diabetes as well as suggest new preventive and therapeutical strategies. METHODS: A standard meal test has been used for monitoring the postprandial concentrations of gastrointestinal hormones and oxidative stress markers in patients with T2D (n = 50) compared to healthy controls (n = 50). Blood samples were drawn 0, 30, 60, 120 and 180 minutes after the standard meal. RESULTS: Both basal and postprandial plasma concentrations of glucose and insulin proved to be significantly higher in patients with T2D, whereas plasma concentrations of ghrelin showed significantly lower values during the whole meal test. In comparison with healthy controls, both basal and postprandial concentrations of almost all other gastrointestinal hormones and lipoperoxidation were significantly increased while ascorbic acid, reduced glutathione and superoxide dismutase activity were decreased in patients with T2D. A positive relationship was found between changes in GIP and those of glucose and immunoreactive insulin in diabetic patients (p<0.001 and p<0.001, respectively) and between changes in PYY and those of glucose (p<0.01). There was a positive correlation between changes in GIP and PYY and changes in ascorbic acid in patients with T2D (p<0.05 and p<0.001, respectively). CONCLUSION/INTERPRETATION: Apart from a positive relationship of postprandial changes in GIP and PYY with changes in ascorbic acid, there was no direct link observed between gastrointestinal hormones and oxidative stress markers in diabetic patients. TRIAL REGISTRATION: ClinicalTrials.gov NCT01572402.

• MeSH
• diabetes mellitus 2. typu krev   MeSH
• gastrointestinální hormony krev   MeSH
• inzulin krev   MeSH
• krevní glukóza analýza   MeSH
• kyseliny mastné neesterifikované krev   MeSH
• lidé středního věku MeSH
• lidé MeSH
• lipidy krev   MeSH
• oxidační stres fyziologie   MeSH
• postprandiální období fyziologie   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• gastrointestinální hormony MeSH
• inzulin MeSH
• krevní glukóza MeSH
• kyseliny mastné neesterifikované MeSH
• lipidy MeSH

AIMS/HYPOTHESIS: The aim of the study was to compare the effect of six (A6 regimen) vs two meals a day, breakfast and lunch (B2 regimen), on body weight, hepatic fat content (HFC), insulin resistance and beta cell function. METHODS: In a randomised, open, crossover, single-centre study (conducted in Prague, Czech Republic), we assigned 54 patients with type 2 diabetes treated with oral hypoglycaemic agents, both men and women, age 30-70 years, BMI 27-50 kg/m(2) and HbA1c 6-11.8% (42-105 mmol/mol), to follow two regimens of a hypoenergetic diet, A6 and B2, each for 12 weeks. Randomisation and allocation to trial groups (n = 27 and n = 27) were carried out by a central computer system. Individual calculations of energy requirements for both regimens were based on the formula: (resting energy expenditure × 1.5) - 2,092 kJ. The diet in both regimens had the same macronutrient and energy content. HFC was measured by proton magnetic resonance spectroscopy. Insulin sensitivity was measured by isoglycaemic-hyperinsulinaemic clamp and calculated by mathematical modelling as oral glucose insulin sensitivity (OGIS). Beta cell function was assessed during standard meal tests by C-peptide deconvolution and was quantified with a mathematical model. For statistical analysis, 2 × 2 crossover ANOVA was used. RESULTS: The intention-to-treat analysis included all participants (n = 54). Body weight decreased in both regimens (p < 0.001), more for B2 (-2.3 kg; 95% CI -2.7, -2.0 kg for A6 vs -3.7 kg; 95% CI -4.1, -3.4 kg for B2; p < 0.001). HFC decreased in response to both regimens (p < 0.001), more for B2 (-0.03%; 95% CI -0.033%, -0.027% for A6 vs -0.04%; 95% CI -0.041%, -0.035% for B2; p = 0.009). Fasting plasma glucose and C-peptide levels decreased in both regimens (p < 0.001), more for B2 (p = 0.004 and p = 0.04, respectively). Fasting plasma glucagon decreased with the B2 regimen (p < 0.001), whereas it increased (p = 0.04) for the A6 regimen (p < 0.001). OGIS increased in both regimens (p < 0.01), more for B2 (p = 0.01). No adverse events were observed for either regimen. CONCLUSIONS/INTERPRETATION: Eating only breakfast and lunch reduced body weight, HFC, fasting plasma glucose, C-peptide and glucagon, and increased OGIS, more than the same caloric restriction split into six meals. These results suggest that, for type 2 diabetic patients on a hypoenergetic diet, eating larger breakfasts and lunches may be more beneficial than six smaller meals during the day. Trial registration ClinicalTrials.gov number, NCT01277471, completed. Funding Grant NT/11238-4 from Ministry of Health, Prague, Czech Republic and the Agency of Charles University - GAUK No 702312.

• MeSH
• C-peptid krev   MeSH
• diabetes mellitus 2. typu krev   dietoterapie   farmakoterapie   MeSH
• dospělí MeSH
• glukagon krev   MeSH
• hypoglykemika terapeutické užití   MeSH
• inzulin krev   MeSH
• jídla * MeSH
• klinické křížové studie MeSH
• krevní glukóza MeSH
• lidé středního věku MeSH
• lidé MeSH
• oběd MeSH
• redukční dieta metody   MeSH
• senioři MeSH
• snídaně MeSH
• výsledek terapie MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• randomizované kontrolované studie MeSH
• Názvy látek
• C-peptid MeSH
• glukagon MeSH
• hypoglykemika MeSH
• inzulin MeSH
• krevní glukóza MeSH