cholecystokinin and Hyperlipidemias

Topics: Animals; Bile; Bile Acids and Salts; Bile Ducts; Blood Protein Disorders; Cholecystokinin; Cholelithiasis; Cholesterol; Female; Gallbladder; Humans; Hyperlipidemias; Lipoproteins, VLDL; Liver; Liver Circulation; Male; Phosphatidylcholines; Phospholipids; Pregnancy; Pregnancy Complications

Sodium-bicarbonated mineral waters are reported to have beneficial digestive and hypocholesterolaemic properties. The aim of the study was to investigate the effects of consumption of a sodium-bicarbonated mineral water (BW) with or without a meal, compared to a low mineral content water as the control water (CW), on postprandial serum triacylglycerols (TAG), cholecystokinin (CCK) and gallbladder volume.. The study design was a four-way randomised controlled crossover trial. Healthy adult men and women (>18 and <40 years, TAG <2.82 mmol/L) consumed 0.5 L of CW + standard meal; 0.5 L of BW + standard meal; and 0.5 L of CW without meal or 0.5 L of BW without meal.. BW consumed without meal had no significant effect on the study parameters compared to CW. However, BW with meal induced a lower concentration of serum TAG at 30 min (p = 0.01) and 60 min (p = 0.03) postprandial times, lower CCK concentrations at 30 min (p = 0.002), and higher gallbladder volume at 30 min (p = 0.03), 60 min (p = 0.01) and 120 min (p = 0.04). Gallbladder ejection fraction was lower with the BW (p = 0.03), whilst area under the curve and peak contraction amplitude (lowest gallbladder volume) were higher (p = 0.01, p = 0.02, respectively) compared to the CW.. Consumption of BW with a meal induces lower levels of CCK and reduces gallbladder emptying and postprandial TAG levels. It is proposed that this sodium-bicarbonated mineral water could be used as part of the habitual diet by the general population in order to reduce cardiovascular risk.

Topics: Adolescent; Adult; Cardiovascular Diseases; Cholecystokinin; Cross-Over Studies; Drinking Water; Female; Gallbladder Emptying; Humans; Hyperlipidemias; Male; Mineral Waters; Postprandial Period; Risk Factors; Sodium Bicarbonate; Triglycerides; Young Adult

Functions of the gut hormone cholecystokinin (CCK) include an important role in the regulation of gastric emptying, postprandial glucose homeostasis, and postmeal satiety. Postprandial CCK responses are significantly blunted in type 2 diabetic patients by unknown mechanisms. We hypothesized that hyperinsulinemia and lipid infusion influence circulating levels of biologically active CCK.. Eleven healthy subjects were studied in a cross-over design after 10-h overnight fasts, using euglycemic-hyperinsulinemic clamps for 443 min, with an additional infusion of lipid-heparin (1.25 ml.min(-1)) or saline (1.25 ml.min(-1)) for the last 300 min after constant plasma glucose levels were achieved.. Euglycemic-hyperinsulinemia resulted in a sustained, up to 5-fold increase of plasma CCK (P < 0.001). When adding lipid infusion instead of saline, CCK concentrations rapidly declined and returned to baseline levels (CCK(300 min) 1.1 +/- 0.2 vs. 3.3 +/- 0.3 pmol/liter, P < 0.001). Partial intraclass correlation showed an independent correlation of plasma CCK with free fatty acids (r(ic) = -0.377, P < 0.001) but not with serum insulin (r(ic) = 0.077, P = 0.32). Whole-body insulin sensitivity decreased in lipid-exposed subjects (M value 7.1 +/- 0.7 vs. 5.6 +/- 0.9 mg.kg.min(-1), P = 0.017) but was not independently correlated with CCK (r(ic) = 0.040, P = 0.61).. We report novel findings showing that circulating CCK markedly increased in the euglycemic-hyperinsulinemic state, possibly as a result of near-complete suppression of circulating free fatty acids. Moreover, raising blood lipids even moderately by lipid infusion rapidly and significantly interfered with this effect, suggesting that a negative feedback mechanism of blood lipids on circulating CCK might exist.

Topics: Cholecystokinin; Cross-Over Studies; Female; Glucose Clamp Technique; Humans; Hyperinsulinism; Hyperlipidemias; Infusion Pumps; Insulin; Insulin Resistance; Lipids; Male; Middle Aged

The aim of the present study was to investigate whether hyperlipidemia can cause acute pancreatitis or alter its severity. Male Wistar rats were fed a 3% cholesterol-enriched diet or a normal diet for 16 weeks. Edematous and necrotizing pancreatitis was induced with 3x75 mug/kg body weight of cholecystokinin s.c. and 2x2 g/kg body weight of L-arginine i.p., respectively, in separate groups of normal and hyperlipidemic rats. The severity of the pancreatitis was assessed. We studied the influence of hyperlipidemia on the formation of oxygen-derived free radicals, endogenous scavengers, nitric oxide synthases (NOS), peroxynitrite (ONOO(-)), heat shock protein 72 (HSP72) and nuclear factor-kappa B (NF-kappaB) activation in the pancreas during acute edematous and necrotizing pancreatitis. Hyperlipidemia did not worsen edematous, but aggravated necrotizing pancreatitis. The cholesterol-enriched diet significantly reduced the catalase and Mn-superoxide dismutase (SOD) and constitutive NOS (cNOS) activities and increased the inducible NOS (iNOS) in the pancreas relative to those in the rats on the normal diet. The pancreatic nitrotyrosine level, as a marker of ONOO(-), and the NF-kappaB DNA-binding activity in the pancreas, were significantly elevated in the cholesterol-fed rats. The pancreatic HSP72 expression during necrotizing pancreatitis was not influenced by the hyperlipidemia. The pancreatic Mn-SOD, Cu, Zn-SOD, glutathione peroxidase, total glutathione and cNOS activities were significantly reduced, while the catalase, iNOS and NF-kappaB DNA-binding activities were significantly increased in the animals with necrotizing pancreatitis on the cholesterol diet as compared with those with pancreatitis and receiving the normal diet. Hyperlipidemia induced with this cholesterol-enriched diet leads to decreases in endogenous scavenger and cNOS activities, results in iNOS and NF-kappaB activation and stimulates ONOO(-) generation in the pancreas, which may be responsible for the aggravation of acute necrotizing pancreatitis.

Topics: Animals; Arginine; Catalase; Cholecystokinin; Cholesterol, Dietary; Free Radical Scavengers; HSP72 Heat-Shock Proteins; Hyperlipidemias; Male; NF-kappa B; Nitric Oxide Synthase; Oxidative Stress; Pancreas; Pancreatitis, Acute Necrotizing; Peroxynitrous Acid; Rats; Rats, Wistar; Superoxide Dismutase

Alpha-lipoic acid (ALA) has been used as an antioxidant. The aim of this study was to investigate the effect of alpha-lipoic acid on cholecystokinin (CCK)-octapeptide induced acute pancreatitis in rats.. ALA at 1 mg/kg was intra-peritoneally injected, followed by 75 microg/kg CCK-octapeptide injected thrice subcutaneously after 1, 3, and 5 h. This whole procedure was repeated for 5 d. We checked the pancreatic weight/body weight ratio, the secretion of pro-inflammatory cytokines and the levels of lipase, amylase of serum. Repeated CCK octapeptide treatment resulted in typical laboratory and morphological changes of experimentally induced pancreatitis.. ALA significantly decreased the pancreatic weight/body weight ratio and serum amylase and lipase in CCK octapeptide-induced acute pancreatitis. However, the secretion of IL-1beta, IL-6, and TNF-alpha were comparable in CCK octapeptide-induced acute pancreatitis.. ALA may have a protective effect against CCK octapeptide-induced acute pancreatitis.

Topics: Acute Disease; Animals; Cholecystokinin; Hyperlipidemias; Injections, Intraperitoneal; Interleukin-1; Interleukin-6; Male; Pancreatitis; Rats; Rats, Wistar; Thioctic Acid; Tumor Necrosis Factor-alpha

Exocrine pancreatic function was tested in 8 patients with pancreatitis and hyperlipoproteinemia type I, IV and V. Three young patients with HLP I and V and 2 patients with alcoholic HLP type V exhibited in most cases a distinctly reduced pancreatic function (chronic relapsing pancreatitis). Three patients with primary or secondary HLP type IV and V did not present pancreatic insufficiency (acute pancreatitis, acute relapsing pancreatitis). Taking into account the literature data and our own experience it can be stated that all forms of excessive hypertriglyceridemia can give rise to acute pancreatitis. Different possible causal relationships between HLP and pancreatitis are discussed. Concomitant occurrence of HLP and pancreatitis is observed most often in alcoholics.

Topics: Adult; Aged; Alcoholism; Cholecystokinin; Female; Humans; Hyperlipidemias; Male; Middle Aged; Pancreatitis; Secretin; Triglycerides

Topics: Acute Disease; Adult; Amylases; Cholecystokinin; Cholesterol; Chylomicrons; Chymotrypsin; Exocrine Glands; Female; Humans; Hyperlipidemias; Lipoproteins; Male; Middle Aged; Pancreas; Pancreatic Diseases; Pancreatitis; Secretin; Triglycerides

Topics: Alcoholism; Amylases; Anemia, Hemolytic; Cholecystokinin; Chymotrypsin; Clinical Enzyme Tests; Fatty Liver; Humans; Hyperlipidemias; Jaundice; Pancreas; Secretin; Trypsin