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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a first study, a population of 1,045 women from 20 to 61 years old has been studies. 24 (2.3%) were known to have gallstones. After excluding these 24 cases, 214 were drawn from the same population and accepted an oral cholecystography. 11 cases of stones (5.1%) were discovered. The diet of these 11 patients and of the 202 women without gallstones was not significantly different. In a second study, the diet of 50 patients with known gallstones and the diet of 50 matched controls have been compared. No significant difference between the two groups can be demonstrated for calories, protein, fat or carbohydrates intake. These results are compared to previous results which showed overconsumption of food in gallstone patients. The method for all studies being similiar, it seems that the dietetic factors are now less important in cholesterol stones pathogenesis than during the period which followed the second world war starvation in southeast France. The assumption that undernutrition diminishes the chance for a women to develop gallstones is proposed.
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PMID:Diet and cholesterol gallstones. A further study. 62 25

Biliary cholesterol saturation indices (SI's) were measured in fasting duodenal bile from (i) obese and non-obese individuals with and without cholesterol gallstones, (ii) obese individuals undergoing weight reduction and (iii) obese gallstone patients receiving chenodeoxycholic acid (CDCA) therapy. Biliary lipid secretion rates were also measured in three obese subjects before and during 11 days starvation. The mean SI in fifteen non-obese controls (0.89 +/- SEM 0.06) was significantly lower than that in the twenty-four obese without (1.14 +/- 0.07; P less than 0.01), and in the twenty-nine non-obese with gallstones (1.30 +/- 0.05; P less than 0.001) while in sixteen obese gallstone patients, the mean SI of 1.55 +/- 0.06 was significantly higher than that seen in the other three groups (P less than 0.01-0.001). Although fifteen obese subjects lost 15% of their initial body weight during dieting, this did not change their SI's consistently. However in three obese individuals, total starvation did reduce the SI's and significantly lowered the biliary cholesterol secretion rate. Ten obese gallstone patients responded to 15.8 +/- 0.3 mg CDCA kg-1 day-1 by developing unsaturated fasting duodenal bile (SI 0.89 +/- 0.04). A further increase in CDCA dose to 19.0 +/- 0.7 mg kg-1 day-1, as a result of reducing body weight, was more effective in lowering SI's (0.75 +/- 0.06, range 0.51-1.0) than that achieved by increasing the dose to 18.9 +/- 0.46 mg kg-1 day-1 through more capsules per day (SI 0.89 +/- 0.03, range 0.67-1.25). These studies show that (i) biliary cholesterol SI's are greater when obesity and gallstones occur together than in either obesity or gallstones alone, and (ii) although weight loss in obese individuals does not consistently alter biliary cholesterol SI's, it may be beneficial in obese patients receiving CDCA therapy for gallstone dissolution.
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PMID:Effect of obesity and weight reduction on biliary cholesterol saturation and the response to chenodeoxycholic acid. 308 8

Regeneration of gallbladder epithelium of rodents is accelerated if a diet inducing cholelithiasis is given, as well as during starvation; both types of dietary regimens have something in common. The increased turnover of mucosal cells and the desquamation of these cells into the lumen of the gallbladder are causative factors for gallstone formation.
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PMID:[Effect of a lithogenic diet and starvation on the regeneration of gallbladder epithelium]. 713 30

The recovery of gastrointestinal electrical activity--migrating myoelectrical complex (MMC) and slow waves--was studied in six women (50-77 years) after cholecystectomy for gallstones: serosal electrodes in pairs are implanted in the wall of the antrum, duodenum and jejunum during surgery. Five hour recordings were made on the first, third and fourth postoperative days (pOD), in starvation condition with hydric intake only. The recordings were made after a twelve hour fast. On the fourth postoperative day, a test meal (250 g yogurt) was given to the patients and its effects on electrical activity were recorded for 2 hours. Even though MMC were present on the first and third postoperative days, a detailed study of their origin, the length of the phase 3 and the speed of gastro-jejunal propagation showed an inhibition of gastric MMC until the fourth pOD, moreover that intestinal MMC was slower than normal until the third pOD. On the fourth postoperative day, gastric inhibition disappeared since the length of the phase 3 of the MMC in the gastric level corresponded to those of the duodenum and jejunum. Furthermore the speed of propagation corresponded to that in normal subjects. Further, the slow wave frequency peculiar to each segment studied increased progressively from the first to the fourth pOD just like the slow waves with action potentials. In conclusion, notwithstanding the presence of MMC from the first postoperative day, it was only on the fourth day that normal coordination was restored and hence that patients were able to eat again.
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PMID:[Recovery of gastroduodenojejunal electric activity after cholecystectomy. In situ study in mam]. 768 87

Abnormal liver tests occur in 1 of 10 pregnancies, though liver function is usually normal during pregnancy. The data suggest that liver metabolic capacity may be reduced in late pregnancy. Hepatic excretory function has been assessed in human pregnancy by both bromosulfophthalein (BSP) and bilirubin tolerance tests. The data suggest that the hepatic excretion of both compounds is impaired in the last half of normal human pregnancy. Thus, the clearance of compounds that are metabolized via the microsomal oxidizing pathway or secreted into bile may be impaired during pregnancy (especially late pregnancy). There is a 20% increase in total body water during pregnancy, and cardiac output increases 30% to 50%. The increment in cardiac output represents shunting of blood to the fetal-placental unit. Serum cholesterol and triglyceride levels begin to rise in the fourth month of pregnancy and peak at term. At term, pregnant women have a 25% to 50% rise in serum cholesterol levels to 265+/-8 mg/dL and a 150% increase in serum triglyceride levels to 180+/-13 mg/dL. Chemical analysis of tissue samples and histologic studies suggest that both cholesterol and triglycerides accumulate in the liver during normal pregnancy. The latter is thought to represent a storage pool of metabolic fuel to sustain the fetus during periods of starvation or inadequate nutrition. It is believed that both the enlarged gallbladder and supersaturation of bile with cholesterol contribute to gallstone formation in pregnant women.
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PMID:Liver problems in pregnancy: distinguishing normal from abnormal hepatic changes. 973 91

We analyzed clinical, biochemical, and histo- logic parameters of ten infants with parenteral nutrition-induced hepatobiliary dysfunction. The data were compared with the results of a rabbit model. All infants were born prematurely with low birth weight. Their clinical diagnoses were necrotizing enterocolitis (6), gastroschisis (1), intrauterine volvulus (1), and lung hypoplasia (2). All required total (TPN) or partial parenteral nutrition for at least 8 weeks. All had repeated episodes of infections or sepsis. A rise in bilirubin and aminotransferase levels occurred after a minimum of 5 weeks; peak bilirubin levels ranged from 4 to 14 mg% and aminotransferases from 40 to 140 IU/l. One child later developed gallstones. Liver biopsies after 1 to 24 months showed fibrosis, bile-duct proliferation, cholestasis, and hydropic degeneration. All of the above-mentioned clinical factors have been accused of causing the observed biochemical and histologic changes. In our rabbit model we were able to produce almost identical symptoms by TPN alone: gallbladder distension, sludge, and stones developed after 1-4 weeks of TPN as well as uncharacteristic changes in aminotransferases and bilirubin after 4 weeks. Liver histology revealed severe hydropic degeneration of zone 3 as early as 1 week after beginning TPN. A rise of fibrosis and bile-duct proliferation after 1 to 4 weeks of infusion was statistically significant. Cholestasis, as was observed in the infants, could not be detected. In our model, all alterations observed could be attributed exclusively to TPN. We therefore assume that TPN was the true cause of the dysfunction. In a second experimental series infusions were reduced to 80% PN and free access to lab chow. These animals produced normal feces, indicating physiologic enteral stimulation. They developed the same degenerative and proliferative histologic changes, whereas gallbladder distension, sludge, and stones were not noted. We conclude that: (1) The TPN solution itself is responsible for the histologic changes in the liver, which is supported by the fact that hydropic degeneration of zone 3 is typical of a direct toxic effect; and (2) Complete enteral starvation with an absence of enteral stimulation causes disease of the lower biliary tract.
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PMID:Parenteral nutrition-induced hepatobiliary dysfunction in infants and prepubertal rabbits. 1052 3

Hepatobiliary dysfunctions (TPN-HBD) occur during parenteral nutrition. In older children these are usually reversible whereas in newborns and infants these hepatobiliary abnormalities play a significant role in the morbidity. Cholestasis is a commonly occurring TPN-HBD. It correlates directly with the decreasing gestational age, low birth weight and increasing duration of TPN therapy. The pathogenesis of cholestasis of TPN is multifactorial and predisposed by necrotising enterocolitis, sepsis, cardiac failure, shock, and hypotension. Diagnosis is made with exclusion of other causes of direct hyperbilirubinemia. Most TPN-HBD appear within 4 weeks of starting of TPN but severe complications manifest usually after the 16th week. Histologically there is intralobular cholestasis. In few cases there may be severe portal fibrosis followed by development of micronodular biliary cirrhosis. Enteral starvation, defective bile acid carriers, hypercaloric TPN are the major factors responsible for TPN-HBD, including cholestasis. Biliary complications of TPN-HBD are acalculous, cholecystitis, and cholelithiasis. Bile stasis is a major pathological factor for these. If the calories are provided only by glucose or glucose-containing electrolyte solutions it may lead to cholestasis and other TPN-HBD. Even small oral alimentation (continuous or bolus) during TPN, prevent TPN-HBD. Choleretic agents have been useful in the prevention and management of cholestasis and other parenteral nutrition induced hepatobiliary abnormalities.
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PMID:Hepatobiliary abnormalities and parenteral nutrition. 1102 27

The biological importance of the aquaporin family of water channels was recently acknowledged by the 2003 Nobel Prize for Chemistry awarded to the discovering scientist Peter Agre. Among the pleiotropic roles exerted by aquaporins in nature in both health and disease, the review addresses the latest acquisitions about the expression and regulation, as well as physiology and pathophysiology of aquaporins in the hepatobiliary tract. Of note, at least seven out of the thirteen mammalian aquaporins are expressed in the liver, bile ducts and gallbladder. Aquaporins are essential for bile water secretion and reabsorption, as well as for plasma glycerol uptake by the hepatocyte and its conversion to glucose during starvation. Novel data are emerging regarding the physio-pathological involvement of aquaporins in multiple diseases such as cholestases, liver cirrhosis, obesity and insulin resistance, fatty liver, gallstone formation and even microparasite invasion of intrahepatic bile ducts. This body of knowledge represents the mainstay of present and future research in a rapidly expanding field.
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PMID:Aquaporins in the hepatobiliary tract. Which, where and what they do in health and disease. 1817 45