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At least 523 records · Page 29Linked to original sources
PubMed1982

Isolated co-lipase deficiency in two brothers.

Two normally developed Assyrian brothers with isolated pancreatic co-lipase deficiency are described. They presented at the age of 5-6 years with loose stools. They had steatorrhoea, and analysis of exocrine pancreatic enzymes in the small intestine showed co-lipase deficiency, while amylase, chymotrypsin, trypsin and lipase were normal. Intraduodenal infusion of purified co-lipase improved fat digestion measured by the triolein breath test. Their steatorrhoea diminished on treatment with enteric-coated pancreatic enzymes.

Bile Acids and Salts↗
PubMed1993

Effect of a satiating meal on the concentrations of procolipase propeptide in the serum and urine of normal and morbidly obese subjects.

The effect of a satiating meal on the serum and urinary concentrations of procolipase propeptide (Ala-Pro-Gly-Pro-Arg, APGPR) immunoreactivity, as measured by enzyme linked immunosorbent assay (ELISA) specific for free APGPR, has been studied in normal and morbidly obese human subjects. The normal subjects displayed a biphasic response with coordinate increases in both serum and urine APGPR immunoreactivity both occurring within the first two hours after the meal. In two of three of the morbidly obese subjects, this early rise in APGPR concentration in urine was not seen but was followed by a slow rise in urinary APGPR immunoreactivity at four to six hours. In both the normal and obese groups, the urinary immunoreactive signal was found to coelute with synthetic APGPR on gel chromatography. In rats, procolipase propeptide (Val-Pro-Asp-Pro-Arg, VPDPR) specifically inhibits fat intake early in the postprandial period when given peripherally or centrally. This study suggests that in humans APGPR reaches the circulation shortly after feeding and is excreted in the urine. These findings are consistent with the hypothesis that human procolipase propeptide may also act as a satiety signal. In addition the late appearance of the peptide in some of the morbidly obese patients could be associated with perturbation of appetite control in these subjects.

Adult↗
PubMed2005

Enterostatin decreases postprandial pancreatic UCP2 mRNA levels and increases plasma insulin and amylin.

This study investigated the chronic effect of enterostatin on body weight and some of the associated changes in postprandial metabolism. Rats were adapted to 6 h of food access/day and a choice of low-fat and high-fat (HF) food and then given enterostatin or vehicle by an intraperitoneally implanted minipump delivering 160 nmol enterostatin/h continuously over a 5-day infusion period. Enterostatin resulted in a slight but significant reduction of HF intake and body weight. After the last 6-h food access period, enterostatin-treated animals had lower plasma triglyceride and free fatty acid but higher plasma glucose and lactate levels than control animals. Enterostatin infusion resulted in increased uncoupling protein-2 (UCP2) expression in various tissues, including epididymal fat and liver. UCP2 was reduced in the pancreas of enterostatin-treated animals, and this was associated with increased plasma levels of insulin and amylin. Whether these two hormones are involved in the observed decreased food intake due to enterostatin remains to be determined. As lipid metabolism appeared to be altered by enterostatin, we measured peroxisome proliferator-activated receptor (PPAR) expression in tissues and observed that PPARalpha, -beta, -gamma1, and -gamma2 expression were modified by enterostatin in epididymal fat, pancreas, and liver. This further links altered lipid metabolism with body weight loss. Our data suggest that alterations in UCP2 and PPARgamma2 play a role in the control of insulin and amylin release from the pancreas. This implies that enterostatin changes lipid and carbohydrate metabolic pathways in addition to its effects on food intake and energy expenditure.

Amyloid↗
PubMed2000

Effect of high-fat diet, surrounding temperature, and enterostatin on uncoupling protein gene expression.

Nonshivering thermogenesis induced in brown adipose tissue (BAT) during high-fat feeding is mediated through uncoupling protein 1 (UCP1). UCP2 is a recently identified homologue found in many tissues. To determine the role of UCP1 and UCP2 in thermoregulation and energy balance, we investigated the long-term effect of high-fat feeding on mRNA levels in mice at two different ambient temperatures. We also treated mice with the anorectic peptide enterostatin and compared mRNA levels in BAT, white adipose tissue (WAT), stomach, and duodenum. Here, we report that high-fat feeding at 23 degrees C increased UCP1 and UCP2 levels in BAT four- and threefold, respectively, and increased UCP2 levels fourfold in WAT. However, at 29 degrees C, UCP1 decreased, whereas UCP2 remained unchanged in BAT and increased twofold in WAT. Enterostatin increased UCP1 and decreased UCP2 mRNA in BAT. In stomach and duodenum, high-fat feeding decreased UCP2 mRNA, whereas enterostatin increased it. Our results suggest that the regulation of uncoupling protein mRNA levels by high-fat feeding is dependent on ambient temperature and that enterostatin is able to modulate it.

Adipose Tissue↗
PubMed1996

Physicochemical characteristics of emulsions during fat digestion in human stomach and duodenum.

Seven fasting subjects were fitted with nasogastric and nasoduodenal tubes and received intragastrically a coarsely emulsified test meal. Gastric and duodenal aspirates were collected after 1, 2, 3, and 4 h. In the duodenum, most lipids (> 90%) were present as emulsified droplets 1-100 microns in size. Large droplets and unemulsified material present in the test meal (> 100 micron) disappeared, whereas smaller droplets (1-50 microns) were generated after 1 h of digestion. Thus the median lipid droplet diameter significantly decreased (19.6 vs. 56.5 microns in the test meal) and the droplet surface area significantly increased (1.58 vs. 0.70 micron2/g fat). Intermediate droplet diameters were 34.3, 46.3, and 27.6 microns after 2, 3, and 4 h, respectively. In the stomach, a comparable emulsion particle size pattern was observed, with median droplet diameters of 17.2, 37.9, 52.4, and 41.6 microns after 1, 2, 3, and 4 h, respectively. However, the extent of triglyceride hydrolysis was much lower in the stomach (6-16%) than in the duodenum (42-45%), where small droplets were enriched in lipolytic products, cholesterol, and phospholipids. The present findings show for the first time that most dietary lipids are present in the human duodenum as emulsified droplets 1-50 microns in size and that no further marked emulsification of dietary fat occurs in the duodenum compared with the stomach.

Adult↗
PubMed1996

Enterostatin efflux in cat intestinal lymph: relation to lymph flow, hyaluronan, and fat absorption.

The question addressed in this study was whether enterostatin, the pancreatic procolipase activation peptide, modulates intestinal hyaluronan turnover via lymph. In anesthetized cats, segments of ileum were surgically isolated from the proximal and distal gut, the draining lymphatic was cannulated, and the segment was autoperfused in situ. In several groups, concentrations of immunoreactive enterostatin in lymph were compared with that in plasma at baseline and elevated lymph flow and in the absence and presence of fat absorption. The baseline ratio of lymph enterostatin to that in plasma (L/P) in the absence of fat absorption was 1.44 +/- 0.29 compared with 4.93 +/- 0.42 after cream feeding (P < 0.05). In a separate group, when the intestinal lumen was perfused for 2 h with a mixture of oleic acid and taurocholate, enterostatin L/P doubled compared with baseline. At high lymph flows, enterostatin concentrations fell in all groups, resulting in an L/P of 0.47 +/- 0.09 (P < 0.05) in the absence of fat absorption, 0.77 +/- 0.35 after oleic acid, and 1.26 +/- 0.13 in the cream-fed group. These changes correlate with the pattern of hyaluronan efflux from the ileum into lymph after fat absorption [R.K. Reed, M.I Townsley, V.H. Pitts, T.C. Laurent, and A.E. Taylor. Am. J. Physiol, 263 (Gastrointest. Liver Physiol. 26): G6-G11, 1992] However, in separate groups when enterostatin was introduced into ileum, either as a close intra-arterial bolus or via the intestinal lumen, there were no resultant changes in efflux of hyaluronan from the intestine into lymph. In conclusion, despite the fact that delivery of pancreatic exocrine secretions to the ileal lumen was blocked in this model, enterostatin concentration in lymph increased after fat absorption. Nonetheless, it seems clear that enterostatin does not modify intestinal hyaluronan turnover.

Animals↗
PubMed1998

Capillary diffusion capacity and tissue distribution of pancreatic procolipase in rat.

The permeability-surface area product of procolipase and its apparent distribution volume in rat tissues were assessed using a tissue uptake technique. Procolipase was investigated together with 51Cr-EDTA, used as an inert extracellular marker, and 131I-albumin, used as a plasma volume marker. The tissue uptake of procolipase seemed to occur by passive transport in most of the organs studied, such as in muscle, liver, lung, adipose tissue, adrenal glands, colon, and skin. However, throughout the gastrointestinal tract, except in the colon, there was a high uptake of procolipase, greatly exceeding that of 51Cr-EDTA. This was especially evident in the stomach, in which the procolipase uptake was nonsaturable within the experimental period. Also, in the central nervous system (CNS), there was evidence of specific, possibly carrier-mediated, transport. These results suggest that procolipase may have specific, conceivably receptor-mediated, transport pathways across the microvascular endothelium in the stomach, pancreas, duodenum, ileum, and the CNS.

Animals↗
PubMed2005

Different metabolic responses to central and peripheral injection of enterostatin.

Enterostatin, a pentapeptide cleaved from procolipase, suppresses fat intake after peripheral and central administration. Chronic treatment of rats with enterostatin decreases body weight and body fat. The effect was greater than could be accounted by the reduction in food intake alone. Hence, we have investigated the effect of enterostatin on energy metabolism. Male Sprague-Dawley rats adapted to a high-fat diet were implanted with lateral cerebral ventricular or amygdala cannulas. The metabolic effects were determined by indirect calorimetry. After habituation to the test cages, fasted rats were injected with either saline vehicle or enterostatin given either intraperitoneally (100 nmol) or intracerebroventricularly (1 nmol) or into specific brain regions [amygdala (0.01 nmol) or paraventricular nucleus (PVN) (0.1 nmol)]. Respiratory quotient (RQ) and energy expenditure were monitored over 2 h. Intraperitoneal enterostatin reduced RQ (saline: 0.81 +/- 0.02 vs. enterostatin: 0.76 +/- 0.01) and increased energy expenditure by 44%. Intracerebroventricular enterostatin increased the energy expenditure without any effects on RQ, whereas PVN enterostatin increased metabolic rate, while preventing the increase in RQ observed in the control animals. In contrast, neither RQ nor energy expenditure was altered after enterostatin was injected into the amygdala. Enterostatin activated AMP-activated protein kinase in primary cultures of human myocytes in a dose- and time-dependent manner and increased the rate of fatty acid beta-oxidation. These findings suggest that enterostatin regulates energy expenditure and substrate partitioning through both peripheral and central effects.

Adenylate Kinase↗
PubMed2003

Enterostatin inhibition of dietary fat intake is dependent on CCK-A receptors.

Enterostatin, a pentapeptide released from the exocrine pancreas and gastrointestinal tract, selectively inhibits fat intake through activation of an afferent vagal signaling pathway. This study investigated if the effects of enterostatin were mediated through a CCK-dependent pathway. The series of in vivo and in vitro experiments included studies of 1) the feeding effect of peripheral enterostatin on Otsuka Long Evans Tokushima Fatty (OLETF) rats lacking CCK-A receptors, 2) the effect of CCK-8S on the intake of a two-choice high-fat (HF)/low-fat (LF) diet, 3) the effects of peripheral or central injection of the CCK-A receptor antagonist lorglumide on the feeding inhibition induced by either central or peripheral enterostatin, and 4) the ability of enterostatin to displace CCK binding in a 3T3 cell line expressing CCK-A receptor gene and in rat brain sections. The results showed that OLTEF rats did not respond to enterostatin (300 microg/kg ip) in contrast to the 23% reduction in intake of HF diet in Long Evans Tokushima Otsuka (LETO) control rats. CCK (1 microg/kg ip) decreased the intake of the HF diet in a two-choice diet regime with a compensatory increase in intake of the LF diet. Peripheral injection of lorglumide (300 microg/kg) blocked the feeding inhibition induced by either near-celiac arterial or intracerebroventricular enterostatin, whereas intracerebroventricular lorglumide (5 nmol icv) only blocked the response to intracerebroventricular enterostatin but not to arterial enterostatin. Enterostatin did not bind on CCK-A receptors because neither enterostatin nor its analogs VPDPR and beta-casomorphin displaced [3H]L-364,718 from CCK-A receptors expressed in 3T3 cells or the binding of 125I-CCK-8S from rat brain sections. The data suggest that both the peripheral and central responses to enterostatin are mediated through or dependent on peripheral and central CCK-A receptors.

3T3 Cells↗
PubMed1998

Chronic ingestion of dietary fat is a prerequisite for inhibition of feeding by enterostatin.

Enterostatin (Ent), the activation pentapeptide from procolipase, inhibits the intake of dietary fat. The selectivity of the response to fat suggests that the rat must recognize a permissive signal related to dietary fat for the Ent biological response. To investigate the nature of this signal, we studied the effects of Ent in rats that were adapted to either a high-fat (HF) or high-carbohydrate/low-fat (HC) diet and then naively exposed to either HF or HC diets. Ent (1 nmol) was injected into the lateral ventricle of overnight-fasted rats, and food intake was measured. Rats adapted to HF diet and tested with HC diet responded to Ent, but rats adapted to HC diet and tested with HF did not respond to Ent. The groups were maintained on their new test diets for up to 21 days and tested again for their response to Ent at 3, 7, 14, and 21 days. Ent response did not appear in HC-adapted rats switched to HF diet before 21 days. Conversely, the HF-adapted rats, which responded to Ent when tested with HC diet for the first time, did not respond at any subsequent testing time. The data suggest that chronic ingestion of dietary fat is required for Ent action and that chronic consumption of fat initiates a postingestion metabolic, endocrine, or neurochemical change that is required for the biological response to Ent.

Acclimatization↗
PubMed2000

Enterostatin suppresses food intake in rats after near-celiac and intracarotid arterial injection.

Enterostatin (Ent) selectively suppresses the intake of dietary fat after peripheral and central administration. To further investigate the site of action of Ent, we compared the feeding responses to Ent injected intra-arterially near the celiac artery, into the carotid artery, or intravenously in rats adapted to a high-fat diet. After near-celiac arterial injection there was an immediate dose-dependent (0.05-13.5 nmol) inhibition of food intake occurring within 5 min in overnight-fasted rats that lasted up to 20 min. Carotid arterial Ent had a similar, immediate dose-related response, and the inhibitory effect was long lasting. The response to intravenous Ent was only evident at the highest dose (13.5 nmol) and was delayed for at least 120 min. Pretreatment with capsaicin, which causes degeneration of vagal sensory neurons, abolished the inhibitory responses to near-celiac Ent but not to intravenous or intracarotid Ent. These results provide further evidence for both a gastrointestinal site of action for peripheral Ent and a central site of action for intracarotid Ent and suggest that the delayed response to intravenous Ent may reflect either binding or slow uptake of this peptide into the central nervous system.

Animals↗
PubMed2002

QTL analysis of self-selected macronutrient diet intake: fat, carbohydrate, and total kilocalories.

The present study investigated the inheritance of dietary fat, carbohydrate, and kilocalorie intake traits in an F(2) population derived from an intercross between C57BL/6J (fat-preferring) and CAST/EiJ (carbohydrate-preferring) mice. Mice were phenotyped for self-selected food intake in a paradigm which provided for 10 days a choice between two macronutrient diets containing 78/22% of energy as a composite of either fat/protein or carbohydrate/protein. Quantitative trait locus (QTL) analysis identified six significant loci for macronutrient intake: three for fat intake on chromosomes (Chrs) 8 (Mnif1), 18 (Mnif2), and X (Mnif3), and three for carbohydrate intake on Chrs 17 (Mnic1), 6 (Mnic2), and X (Mnic3). An absence of interactions among these QTL suggests the existence of separate mechanisms controlling the intake of fat and carbohydrate. Two significant QTL for cumulative kilocalorie intake, adjusted for baseline body weight, were found on Chrs 17 (Kcal1) and 18 (Kcal2). Without body weight adjustment, another significant kcal locus appeared on distal Chr 2 (Kcal3). These macronutrient and kilocalorie QTL, with the exception of loci on Chrs 8 and X, encompassed chromosomal regions influencing body weight gain and adiposity in this F2 population. These results provide new insight into the genetic basis of naturally occurring variation in nutrient intake phenotypes.

Animals↗
PubMed1996

Changes in plasma insulin, enterostatin, and lipoprotein levels during an energy-restricted dietary regimen including a new oat-based liquid food.

The changes in plasma insulin, enterostatin, lipid, and glucose levels during weight reduction were studied in 32 subjects having a body mass index of 25-35. The 31 subjects who completed the study followed for 23 weeks an energy-restricted dietary regimen which included a new oat-based soup as the main meal once or twice daily. The intake of energy decreased from 8.9 to 6.2 MJ/day from 0 to 22 weeks, the energy percentage from fat decreased from 35 to 30%, and the intake of dietary fiber increased from 21 to 25 g/10 MJ. The body weight decreased from 83 to 78 kg after 6 weeks and to 77 kg after 23 weeks. Plasma glucose had decreased significantly from 5.4 to 5.2 mmol/l, and plasma insulin from 122 to 98 pmol/l after 23 weeks. In contrast, the plasma enterostatin concentration did not vary significantly over five sampling times, the mean values ranging from 25 to 30 nmol/l. Plasma cholesterol declined from 5.6 to 5.2 mmol/l, low-density lipoprotein cholesterol from 3.8 to 3.3, and plasma triglycerides from 1.5 to 1.3 mmol/l from 0 to 23 weeks. High-density lipoprotein cholesterol increased from 1.1 to 1.3 mmol/l. It is concluded that an energy-restricted regimen leading to lower plasma insulin, triglyceride, and low-density lipoprotein cholesterol levels did not significantly affect the plasma enterostatin concentration in overweight subjects. A new oat-based liquid food as a part of the dietary regimen was well tolerated.

Adult↗