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PubMed1992

Regulation of intestinal apo A-IV mRNA abundance in rat pups during fasting and refeeding.

The amount of intestinal apolipoprotein (apo) A-IV mRNA was examined in rat pups during fasting and refeeding. When 14-day old pups were fasted for 15 h, apo A-IV mRNA levels in the whole intestine decreased to 20% of the prefasting level. Refeeding casein and lactose, and the artificial milk composed of Intralipid, casein and lactose, caused an elevation of the apo A-IV mRNA after 3 h, without accompanying an elevation of serum triacylglycerols and apo A-IV (fat-independent elevation of apo A-IV mRNA). Refeeding Intralipid alone simultaneously elevated the apo A-IV mRNA, and serum triacylglycerols and apo A-IV after 3 h (fat-dependent elevation of apo A-IV mRNA). Administration of physiological saline during fasting partly suppressed the reduction of the apo A-IV mRNA (40% of the prefasting level), and the dietary fat-independent elevation of the message disappeared. Refeeding dam's milk to the pups, fasted without water administration, increased the apo A-IV mRNA after 3 and 15 h, although the elevation of serum triacylglycerols and apo A-IV occurred only after 15 h. Refeeding the milk increased the apo A-IV mRNA after 3 h and 15 h. Refeeding dam's milk to the pups fasted with saline administration accelerated the fat-dependent elevation of the apo A-IV mRNA. Simultaneously refeeding Intralipid and Pluronic L-81, an inhibitor of lymphatic fat transport, delayed the elevation of the apo A-IV mRNA and serum triacylglycerols and apo A-IV. Transcription rates of the apo A-IV mRNA, determined by nuclear run/on assay, were similar before and after fasting and refeeding Intralipid. During fasting, administration of puromycin, as compared with actinomycin D, enhanced the disappearance rate of the apo A-IV message. Intestinal mRNA for apo B, but not for apo A-I and beta-actin, similarly changed to the apo A-IV message. Thus, it can be concluded that: (1) dietary fat-dependent and -independent factors are involved in the elevation of the intestinal apo A-IV message; (2) the elevation of the message is not mediated by lipid uptake in the enterocytes but rather stimulated by the events leading to secretion of chylomicrons; and, (3) dietary fat-dependent elevation of the message appears to be due to the stabilization of the message.

Animals↗
PubMed1985

The concentration of blood components related to fuel metabolism during prolonged fasting in children.

In order to study the relationship between sex, age and glucose, and the concentrations of various fuel related blood substrates in children during prolonged fasting, we have selected data of fasting procedures in 13 control children aged 3-5 yr, fasted 24 h, and 58 control children aged 6-15 yr, fasted 40 h. Compared to the blood results after overnight fast, glucose is decreased, and lactate, pyruvate, ketones and non-esterified fatty acids (NEFA's) are all clearly increased at the end of fast. The concentrations of alanine and triglycerides remain unchanged. The relation with sex, age and glucose has only been analyzed in the older children group. A sex-dependency is indicated for the ketones. Ketones are negatively related with age. NEFA's pyruvate and alanine are not age-related, whereas glucose, lactate and triglycerides are moderately age-dependent. Ketones are negatively related with glucose, whereas pyruvate, NEFA's and triglycerides are not glucose-related. Lactate and alanine are weakly related to glucose. The data demonstrate diminished glucose homeostasis and increased ketogenesis in younger children compared to older ones during prolonged fasting.

Adolescent↗
PubMed1984

The effect of fasting on the stereotyped behaviour induced by amphetamine and by apomorphine in the albino rat.

Fasting increases the synthesis and metabolism of cerebral 5-hydroxytryptamine and modifies dopamine turnover in the striatum. We studied the effect of a 24 h fast on the motor hyperactivity induced by amphetamine or by apomorphine. Locomotion was evaluated in photocell cages and stereotypy by direct observation and the use of rating scales. Amphetamine, 2.0 mg/kg, induced and increase in locomotion with a maximum between 20 and 30 min of its injection. After 40 min there was a decay in the amphetamine effect but the reduction was significantly smaller in the fasted than in the fed rats. Haloperidol, 0.025 mg/kg, abolished the decay of the amphetamine effect mentioned above and also eliminated the difference between fasted and fed rats. The stereotypy effect of amphetamine was of similar intensity in both groups during the first 30 min after the injection. After 40 min however, fasted rats developed a less intense stereotypy effect than did fed rats. Haloperidol induced a pronounced reduction of stereotypy in both groups and abolished the difference between fasted and fed rats. The stereotypy effect of apomorphine was unaffected by fasting. We suggest that food deprivation reduces the stereotypy effect of amphetamine by acting at a presynaptic dopaminergic level in the striatum.

Animals↗
PubMed1983

Schistosoma mansoni, S. japonicum, S. haematobium: glycogen content and glucose uptake in parasites from fasted and control hosts.

The glycogen content of male and female Schistosoma mansoni has been measured in flukes from normally fed hosts and those from fasted hosts. In infections from both the mouse and the hamster, a significant reduction in schistosomal glycogen of males is seen hours after food is withdrawn from the host. Reductions in protein content of the schistosomes were only observed in hamster infections fasted at least 72 hr. The livers of infected mice not only decrease in size during fasting, but there is a concomitant reduction in glycogen per unit wet weight. Comparisons of glycogen:protein ratios of mansonian males, females, and host livers indicate that the fasting-induced loss of liver glycogen is also observed in the male schistosome, but not the female. Studies of both S. mansoni and S. haematobium pairs from fed hosts suggest that the ratio of glycogen:protein contents in the male schistosome correlates with the glycogen:protein ratio of the female partner. Measurements of glucose uptake in vitro suggest that greater uptake rates may be observed in flukes perfused from fasted hosts. In S. japonicum from infected mice, a reduction in male glycogen was also detected as early as after a 6-hr fasting period, but changes in the females were not significant. Unmated male S. japonicum also exhibit a reduction in glycogen levels after fasting, but the quantity of worm glycogen present in these males remains higher than comparable mated males. In mice entrained to a regulated pattern of available food, fluctuations in glycogen content of the male schistosomes were observed, but in the female partners fluctuations were of a smaller magnitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Hepatic bilirubin and UDP-glucuronate levels in Bolivian squirrel monkeys exhibiting fasting hyperbilirubinemia.

1. Bolivian squirrel monkeys (BoSMs), which are animal models for Gilbert's syndrome, have 40% less hepatic bilirubin UDP-glucuronyltransferase (BR-UPPG-T) activity than Brazilian squirrel monkeys (BrSMs). 2. Although fasting results in similar decreases in hepatic UDP-glucose and UDP-glucuronate levels in both simian subspecies, increased activities (55%) of BR-UDPG-T are induced only in the fasted control BrSMs, which do not exhibit the marked fasting hyperbilirubinemia (FH). 3. Total hepatic bilirubin (BR) concentrations were 50% greater in both fed and fasted BoSMs when compared to BrSMs. 4. Hepatic unconjugated BR levels increase upon fasting only in Gilbert-like BoSMs, reaching concentrations twice that observed in BrSMs. 5. Elevated hepatic BR levels in fasted BoSMs may reflect BR overproduction or inadequate glucuronidation. 6. The increased BR-UDPG-T activity induced in BrSMs during fasting could compensate in-part for the UDPGA depletion and prevent the marked FH as observed in BoSMs.

Animals↗
PubMed1984

Effects of fasting and aminophylline on norepinephrine-stimulated non-shivering thermogenesis.

In an attempt to further elucidate the mechanisms of fasting-depressed maximum thermogenesis and cold tolerance, norepinephrine (NE)-stimulated non-shivering thermogenesis (NST) in cold-acclimated rats was used as a functional index of possible alterations in adrenergic efficacy after fasting. Fasting decreased the magnitude of maximum NE-Stimulated NST by 18.2% [6.87 +/- 0.47 Kcal (Kg X 75 X min)-1 well-fed vs. 5.81 +/- 0.39 Kcal (Kg X 75 X min)-1 fasted], but the apparent adrenergic binding affinity was not affected [Ke = 0.43 micrograms NE min-1 well-fed vs. 0.55 micrograms NE min-1 fasted]. Pretreatment with aminophylline [15 mg Kg-1, i.p.], a phosphodiesterase inhibitor, restored the fasting-depressed NE-stimulated NST to the fed level. The results suggest that the depression of maximum thermogenesis after fasting is not due to changes in adrenergic binding characteristics but to alteration in cAMP production/degradation, resulting in decreased substrate mobilization for thermogenesis.

Aminophylline↗
PubMed1985

Altered distribution and toxicity of digitoxigenin in fasted mice.

Intravenous administration of digitoxigenin (DTXGN) evokes seizure episodes in mice which may be dependent on brain biogenic amines such as serotonin (5-HT). Fasting is known to have effects on both drug toxicity and brain 5-HT synthesis. The purpose of this study was to assess the effects of overnight fasting on DTXGN toxicity. The i.v. LD-50 of DTXGN was increased by 61% in fasted mice. Adjustment of DTXGN dose for the decrease in body weight of fasted mice did not alter the fasting induced protection. A loading dose of 1-tryptophan (25 mg/kg, i.p.) did not alter mortality rates in either fed or fasted mice. Cortical levels of 3H-DTXGN were decreased significantly by 25% in fasted mice. Liver and blood levels were elevated significantly. These data suggest that decreased DTXGN toxicity is associated with a decrease in its distribution to the cerebral cortex and emphasize the importance of acute dietary status in the expression of drug toxicity.

Animals↗
PubMed1977

Mechanism of glucose intolerance during fasting: differences between lean and obese subjects.

Oral glucose tolerance tests were performed on 14 lean and 14 obese nondiabetic subjects before and after a 6-day fast. In addition, insulin tolerance tests were performed on 8 lean and 8 obese subjects before and after starvation. Both in lean and obese subjects glucose tolerance deteriorated during starvation, but much more so in the lean population. During fasting, insulin elevation after a glucose load was significantly delayed in lean subjects but not in the obese. Circulating levels of factors known to affect glucose tolerance, such as glucagon, growth hormone, free fatty acids, and ketone bodies were higher in fasting lean than in fasting obese individuals. In normals fasting resulted in a significant decrease of the blood glucose response to insulin injection, whereas in fasting obese subjects glucose response was unchanged. The results obtained suggest that the effect of fasting on insulin release and insulin sensitivity was more pronounced in lean than in obese subjects, which resulted in greater deterioration of glucose tolerance in the lean population.

Adult↗
PubMed1977

The effects of prolonged fasting on plasma triglyceride kinetics in man.

Studies were undertaken to examine triglyceride turnover in obese humans on isocaloric balanced diets and during prolonged (3-5 wk) fasting. The data were related to plasma concentrations of insulin (IRI), glucagon (IRG), and free fatty acids (FFA) and to blood ketone concentrations. The triglyceride turnover rates were also related to the plasma triglyceride concentration. This relationship was the same in the obese on isocaloric balanced diets as that we have previously observed in lean humans on similar diets. The relationship between triglyceride turnover and concentration changed during prolonged fasting in a way that suggested that triglyceride removal was impaired. This viewpoint is consistent with the known effects of fasting on adipose tissue lipoprotein lipase activity. In another group of fasted obese, refed with a hypocaloric diet, the relationship returned toward normal. In addition to the impaired triglyceride removal, prolonged fasting resulted in a decrease in triglyceride production. This decrease occurred despite an increase in plasma FFA. After 3-5 wk of fasting the IRI was about 50% of the initial value, while the IRG was the same as the initial value. While triglyceride production fell during fasting, the blood ketone concentration rose. Others have seen similar changes in ketones and triglycerides in livers perfused with medium in which the ratio of insulin to glucagon fell. The rate of triglyceride production was not related to body weight. However, regardless of nutritional state, it was positively related to the basal plasma insulin levels. These data indicate that, in man as in animal preparations, insulin may regulate hepatic triglyceride production.

Diet, Reducing↗
PubMed1979

Fasting as a provocative test in neuromuscular diseases.

A 38-hr fast was used as a provocative test in patients suspected of having defects in muscle substrate utilization. In five controls and nine patients, exercise capacity and respiratory exchange ratio were determined before and at the end of the fast. Blood was collected at intervals during the fast from ten controls and nine patients for creatine kinase (CK), free fatty acids, (FFA) beta-hydroxybutyrate, acetoacetate, free and total carnitine, glucose, and alanine. Two patients with myophosphorylase deficiency had increased exercise capacity, and a marked fall in CK, and one had a lesser fall in blood glucose than normal at the end of the fast. Two patients with known lipid myopathies (carnitine deficiency and carnitine palmityl transferase deficiency) had decreased exercise capacity and apparent increased dependence on carbohydrate metabolism during the fast. Carnitine concentrations became even more abnormal in the patient with carnitine deficiency during fasting. Several patients with less well-defined defects were also significantly different from the controls in several respects, indicating that the fast might be useful for finding new defects.

Adult↗
PubMed1987

Increased gonadotropin responsiveness to gonadotropin-releasing hormone during fasting in normal subjects.

To investigate whether food deprivation affects hormone release from pituitary gonadotrophs, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) responses to intravenous (IV) administration of 50 micrograms gonadotropin-releasing hormone (GnRH) were determined in 12 healthy subjects (six women and six men) after an overnight fast and after a fasting period of 56 hours. In the female participants, these GnRH tests were performed early in the follicular phase of the menstrual cycle. Blood glucose declined during the fast from 4.4 +/- 0.1 (mean +/- SEM) to 3.3 +/- 0.1 mmol/L (P less than .001). LH and FSH responsiveness to GnRH--as reflected by hormone incremental areas--increased from 1973 +/- 256 to 3267 +/- 450 (IU/L X min) for LH (P less than .001), and from 376 +/- 44 to 705 +/- 112 (IU/L X min) for FSH (P less than .01). When control studies were carried out in nonfasted subjects in exactly the same way as in the fasted participants, the gonadotropin responsiveness to GnRH did not change significantly between the tests. To explore possible mechanisms behind the increased gonadotropin responsiveness in fasted subjects, six of the above mentioned healthy women were given nine small oral doses of glucose (each dose 0.5 g/kg) during an additional 56-hour fast to prevent blood glucose from falling significantly during the period of food deprivation. This did not change the hormone response pattern at all, since both the LH and the FSH responses to GnRH increased significantly during the glucose-supplemented fasting period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Insulin secretion in the isolated islets of single-, regular-fasted and fed rats.

To investigate the alterations in insulin secretion induced by habituation to single daily meal, adult rats were trained on a regular-fasting scheme (2-hr feeding/22-hr fasting) for 4 weeks. Insulin secretion induced by nutrient secretagogues (D-glucose and L-leucine) and the rates of 45Ca2+ outflow and 14C-glucose oxidation were studied in isolated islets obtained from these animals and in fed and 22-hr single-fasted rats. As expected, in the 22-hr fasted group, insulin secretion was drastically decreased although not abolished while 45Ca2+ outflow and 14C-glucose oxidation rates were only partially reduced. However, the regular-fasted rats did not secrete insulin in response to the nutrient secretagogues; calcium entry was not detected although a partial reduction in 14C-glucose oxidation rate was observed. These results suggest that regular fasting induces alterations in pancreatic B-cell glycolytic pathways leading to impairment of calcium efflux and insulin secretion. Such impairment is more pronounced than that induced by a single 22-hr fast.

Animals↗
PubMed1991

Hepatotoxicity of microcystin-LR in fed and fasted rats.

The LD50 (25 hr, i.p.) for microcystin-LR in fed rats (122 micrograms/kg) was significantly higher than that in fasted rats (72 micrograms/kg). At doses of 100, 150 and 200 micrograms of microcystin-LR per kg, the median times to death were 31.9, 18.2 and 11.2 hr for fed rats, and 1.8, 1.7 and 1.5 hr for fasted rats. A sublethal dose of microcystin (50 micrograms/kg) afforded protection to fasted, but not fed, rats against a subsequent lethal dose (200 micrograms/kg) challenge given 72 hr later. Biochemical and ultrastructural changes resulting from microcystin-LR (100 micrograms/kg, i.p.) were compared in fed and fasted rats 1 hr after injection. In both groups, liver weight and serum levels of sorbitol dehydrogenase and glucose significantly increased. Plasma membranes, isolated from livers of fed or fasted rats, exhibited similar toxin-induced changes in associated cytoskeletal elements. Liver mitochondria from toxin-treated, fasted rats exhibited complete inhibition of state 3 respiration, while those from toxin-treated, fed rats had ADP/O ratios and respiratory control indices comparable to control values. The primary event responsible for enhanced microcystin hepatotoxicity in the fasted state has not yet been identified. Depletion of glycogen stores and a decreased respiratory capacity may, however, play significant roles in this degenerative process.

Animals↗
PubMed1993

Fasting enhances the effects of anoxia on ATP, Cai2+ and cell injury in isolated rat hepatocytes.

The effect of fasting and anoxia on the intracellular concentration of ATP, Na+, Ca2+, Mg2+, and H+ was studied in isolated perfused rat hepatocytes. ATP and intracellular Mg2+ were measured by 31P-NMR spectroscopy, cytosolic free calcium was measured with aequorin, intracellular Na+ with SBFI, intracellular pH with BCECF, lactic dehydrogenase by NADH absorbance. In hepatocytes from fasted rats, intracellular ATP was depressed 52% (P < 0.001), Nai+ was increased 70% from 16.9 to 27.7 mM (P < 0.02), and Cai2+ was increased 79% from 137 to 245 nM (P < 0.05) when compared to fed rats. Mgi2+ and pHi were unchanged. During anoxia, ATP and the cell phosphorylation potential decreased 90% to practically the same low levels in both fed and fasted groups. On the other hand, in hepatocytes from fasted animals, Cai2+ increased faster and to significantly higher levels than in hepatocytes from fed rats: Cai2+ reached 2.19 microM in 10 min compared to 1.45 microM in 1 h, respectively (P < 0.05). Cell injury assessed by LDH release and trypan blue exclusion also occurred earlier and was more severe in hepatocytes from fasted rats. Fructose and Ca(2+)-free perfusion reduced the rise in Cai2+, abolished LDH release and significantly improved the cell viability measured by Trypan blue exclusion. The data demonstrate that fasting decreases the hepatocytes energy potential and increases Nai+ and Cai2+ which are inversely related to the cell energy potential. Consequently, in hepatocytes isolated from fasted rats, the increase in Cai2+ and the resulting cell injury evoked by anoxia occur earlier and are more severe than in fed rats. These results suggest that Ca2+ plays a crucial role in the development of anoxic cell injury.

Adenosine Triphosphate↗
PubMed1988

Effects of the acetylcholinesterase inhibitor pinacolyl methylphosphonofluoridate (soman) on selected endocrine, glucose, and catecholamine levels in fasted and fed rats.

Fed and 18-h fasted rats were given acute doses of either saline or the acetylcholinesterase inhibitor pinacolyl methylphosphonofluoridate (soman) 40, 60, or 80 micrograms/kg. After 30 min plasma samples were collected and assayed for glucose, insulin, glucagon, corticosterone, epinephrine and norepinephrine and the hypothalamus was isolated and assayed for acetylcholinesterase activity. Toxic sign scores were determined and they indicated that soman may be more toxic in the fasted rat. Soman-induced increases in corticosterone were observed in both fasted and fed rats; these levels were significantly higher in fasted rats given either soman or saline. Also, soman-induced increases in glucagon were more pronounced in fasted rats. Soman also caused an apparent dose-dependent increase in catecholamines and a decrease in hypothalamic acetylcholinesterase activity in both groups of rats. The expected lower insulin and glucose levels in the fasted rats were present in the saline-dosed animals and remained lower than fed rats after each dose of soman. This lack of soman-induced hyperglycemia may contribute to the toxicity of soman in fasted rats.

Animals↗
PubMed2004

Preprocedural fasting and adverse events in procedural sedation and analgesia in a pediatric emergency department: are they related?

STUDY OBJECTIVE: Fasting time before procedural sedation and analgesia in a pediatric emergency department (ED) was recently reported to have no association with the incidence of adverse events. This study further investigates preprocedural fasting and adverse events. METHODS: Data were analyzed from a prospectively generated database comprising consecutive sedation events from June 1996 to March 2003. Comparisons were made on the incidence of adverse events according to length of preprocedural fasting time. RESULTS: Two thousand four hundred ninety-seven patients received procedural sedation and analgesia. Four hundred twelve patients were excluded for receiving oral or intranasal drugs (n=95) or for receiving sedation for bronchoscopy by nonemergency physicians (n=317). A total of 2,085 patients received parenteral sedation by emergency physicians. Age range was 19 days to 32.1 years (median age 6.7 years); 59.9% were male patients. Adverse events observed included desaturations (169 [8.1%]), vomiting (156 [7.5%]), apnea (16 [0.8%]), and laryngospasm (3 [0.1%]). Fasting time was documented in 1,555 (74.6%) patients. Median fasting time before sedation was 5.1 hours (range 5 minutes to 32.5 hours). When the incidence of adverse events was compared among patients according to fasting time in hours (0 to 2, 2 to 4, 4 to 6, 6 to 8, >8, and not documented), no significant difference was found. No patients experienced clinically apparent aspiration. CONCLUSION: No association was found between preprocedural fasting and the incidence of adverse events occurring with procedural sedation and analgesia.

Adolescent↗
PubMed2004

Effects of fasting on serum lipids and lipoprotein profiles in the egg-laying hen (Gallus domesticus).

The effects of a 24-h fast on serum lipids and lipoprotein profiles in commercial laying hens were investigated. Blood was analyzed at 34 and 46 weeks of age from Single Comb White Leghorn hens that had been either fed ad libitum or had been fasted for 24 h prior to collection. At 12 weeks, birds were divided into 16 biological isolation units, with 8 replicate units assigned to each treatment group. Four birds out of 10 in each unit were tagged for bleeding. Parameters evaluated included total serum cholesterol and triglycerides, mean diameters of very low density lipoproteins (VLDLs) for the 10th, 50th, and 90th percentiles of serum total VLDL, mean total population VLDL particle diameter (MPD), and percentage serum cholesterol recovered in VLDL, low density lipoprotein (LDL), and high density lipoprotein (HDL) fractions. Fasting led to decreases in total serum cholesterol and triglycerides, and a decrease in mean serum VLDL particle diameter in the 90th population percentile. At Week 34, percentage serum cholesterol recovered from LDL was increased, whereas percentage serum cholesterol recovered from HDL was decreased due to fasting. At Week 46, MPD and percentage serum cholesterol recovered from VLDL were decreased, whereas percentage serum cholesterol recovered from HDL was increased due to fasting. It was concluded that a 24-h fast decreased serum lipids (cholesterol and triglycerides) and the size of VLDL particles in the 90th population percentile in commercial laying hens. Furthermore, bird age influenced the effects of a 24-h fast on MPD and the redistribution of serum cholesterol among VLDL, LDL, and HDL particles.

Animals↗
PubMed2004

Glycogenolysis during short-term fasting in malaria and healthy subjects--the potential regulatory role of glycogen content on glycogen breakdown: a hypothesis.

BACKGROUND & AIMS: During short-term starvation (< 24 h), glucose production decreases 10-20% due to a decrease in glycogenolysis. In the fed state glycogen regulates its rate of breakdown, in order to limit glycogen accumulation. Whether in the fasted state a similar mechanism exists to preserve glycogen content is not known. In malaria, the rate of glycogen breakdown after an overnight fast is considerably lower than in healthy subjects. If glycogen content regulates its rate of breakdown during fasting, we postulate that the rate of glycogenolysis should decrease faster in patients with malaria than in healthy subjects. METHODS: In six non-severe falciparum malaria patients and 6 healthy controls glucose production with [6,6-2H2]-glucose, and glycogenolysis was calculated after measuring gluconeogenesis with the 2H2O-method between 16 and 22 h of fasting. RESULTS: Glucose production after 16 h of fasting was 15% higher in the malaria patients than in controls. Glycogenolysis in the malaria patients was 2.3 +/- 0.37 and 8.4 +/- 0.93 micromol/kg/min in the controls. The absolute decrease in glycogenolysis was slower in malaria patients than in controls (P = 0.001), whereas the relative decrease in glycogenolysis from baseline was not different. CONCLUSION: During fasting the relative decrease in glycogenolysis is independent of the absolute rate of glycogenolysis. The regulation of glycogenolysis during fasting seems not preferentially dictated by glycogen content but, at least in subjects with a low (presumed) glycogen content, driven by the necessity to guarantee glucose output and maintain euglycemia.

Adult↗