Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FASTING”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed1995

[Fast and ultra-fast MRI imaging of the heart].

Conventional magnetic resonance imaging (MRI) is capable of providing satisfactory morphological images of the heart and the surrounding structures. It has further evolved into a well accepted modality for functional cardiac studies such as flow quantification and volumetry. MRI has, however, been hampered by long image acquisition times. This combined with its non-real-time nature and the limited spatial resolution hs made it difficult to extend MRT to the study of small cardiac structures. Recent technical improvements have made breath-held or real-time MRI feasible and thus laid the foundations for further applications in the field of cardiovascular imaging, notably MR coronary angiography, imaging of cardiac valve leaflets, as well as first-pass perfusion studies. Moreover ultrafast MR techniques may eventually replace conventional data acquisition strategies and thus drastically increase patient throughput by shortening acquisition time. This article provides an overview of the technical advances in MRI and their application to the cardiovascular system and discusses possibilities of combined ultrafast and interventional strategies.

Echo-Planar Imaging↗
PubMed2001

The protein-retaining effects of growth hormone during fasting involve inhibition of muscle-protein breakdown.

The metabolic response to fasting involves a series of hormonal and metabolic adaptations leading to protein conservation. An increase in the serum level of growth hormone (GH) during fasting has been well substantiated. The present study was designed to test the hypothesis that GH may be a principal mediator of protein conservation during fasting and to assess the underlying mechanisms. Eight normal subjects were examined on four occasions: 1) in the basal postabsorptive state (basal), 2) after 40 h of fasting (fast), 3) after 40 h of fasting with somatostatin suppression of GH (fast-GH), and 4) after 40 h of fasting with suppression of GH and exogenous GH replacement (fast+GH). The two somatostatin experiments were identical in terms of hormone replacement (except for GH), meaning that somatostatin, insulin, glucagon and GH were administered for 28 h; during the last 4 h, substrate metabolism was investigated. Compared with the GH administration protocol, IGF-I and free IGF-I decreased 35 and 70%, respectively, during fasting without GH. Urinary urea excretion and serum urea increased when participants fasted without GH (urea excretion: basal 392 +/- 44, fast 440 +/- 32, fast-GH 609 +/- 76, and fast+GH 408 +/- 36 mmol/24 h, P < 0.05; serum urea: basal 4.6 +/- 0.1, fast 6.2 +/- 0.1, fast-GH 7.0 +/- 0.2, and fast+GH 4.3 +/- 0.2 mmol/1, P < 0.01). There was a net release of phenylalanine across the forearm, and the negative phenylalanine balance was higher during fasting with GH suppression (balance: basal 9 +/- 3, fast 15 +/- 6, fast-GH 17 +/- 4, and fast+GH 11 +/- 5 nmol/min, P < 0.05). Muscle-protein breakdown was increased among participants who fasted without GH (phenylalanine rate of appearance: basal 17 +/- 4, fast 26 +/- 9, fast-GH 33 +/- 7, fast+GH 25 +/- 6 nmol/min, P < 0.05). Levels of free fatty acids and oxidation of lipid decreased during fasting without GH (P < 0.01). In summary, we find that suppression of GH during fasting leads to a 50% increase in urea-nitrogen excretion, together with an increased net release and appearance rate of phenylalanine across the forearm. These results demonstrate that GH-possibly by maintenance of circulating concentrations of free IGF-I--is a decisive component of protein conservation during fasting and provide evidence that the underlying mechanism involves a decrease in muscle protein breakdown.

Adult↗
PubMed1986

Relationships between insulin and glucose metabolism and pituitary-ovarian functions in fasted heifers.

The effects of fasting between Days 8 and 16 of the estrous cycle on plasma concentrations of luteinizing hormone (LH), progesterone, cortisol, glucose and insulin were determined in 4 fasted and 4 control heifers during an estrous cycle of fasting and in the subsequent cycle after fasting. Cortisol levels were unaffected by fasting. Concentrations of insulin and glucose, however, were decreased (p less than 0.05) by 12 and 36 h, respectively, after fasting was begun and did not return to control values until 12 h (insulin) and 4 to 7 days (glucose) after fasting ended. Concentrations of progesterone were greater (p less than 0.05) in fasted than in control heifers from Day 10 to 15 of the estrous cycle during fasting, while LH levels were lower (p less than 0.01) in fasted than in control heifers during the last 24 h of fasting. Concentrations of LH increased (p less than 0.01) abruptly in fasted heifers in the first 4 h after they were refed on Day 16 of the fasted cycle. Concentrations (means +/- SEM) of LH also were greater (p less than 0.05) in fasted (11.2 +/- 2.6 ng/ml) than in control (4.7 +/- 1.2 ng/ml) heifers during estrus of the cycle after fasting; this elevated LH was preceded by a rebound response in insulin levels in the fasted-refed heifers, with insulin increasing from 176 +/- 35 pg/ml to 1302 +/- 280 pg/ml between refeeding and estrus of the cycle after fasting. Concentrations of LH, glucose and insulin were similar in both groups after Day 2 of the postfasting cycle. Concentrations of progesterone in two fasted heifers and controls were similar during the cycle after fasting, whereas concentrations in the other fasted heifers were less than 1 ng/ml until Day 10, indicating delayed ovulation and (or) reduced luteal function. Thus, aberrant pituitary and luteal functions in fasted heifers were associated with concurrent fasting-induced changes in insulin and glucose metabolism.

Animals↗
PubMed2004

Effect of short-term fasting on plasma concentrations of leptin and other hormones and metabolites in dairy cattle.

We determined the effects of short-term fasting and refeeding on temporal changes in plasma concentrations of leptin, insulin, insulin-like growth factor- 1 (IGF-1), growth hormone (GH), glucose, and nonesterified fatty acids (NEFA), in early lactating cows, non-lactating pregnant cows, and postpubertal heifers. In experiment 1, Holstein cows in early lactation were either fed ad libitum (Control, n=5) or feed deprived for 48 h (Fasted, n=6). Plasma leptin, insulin, and glucose concentrations rapidly declined (P<0.05) within 6h, and IGF-1 by 12h, but all these variables sharply returned to control levels (P>0.10) within 2h of refeeding. Plasma NEFA and GH concentrations were elevated (P<0.05) by 4 and 36 h of fasting and returned to control levels (P>0.10) by 8 and 24h after refeeding, respectively. In experiment 2, four ruminally cannulated pregnant non-lactating Holstein cows were used in a cross-over design and were fasted for 48 h (Fasted) or fasted with partial evacuation of rumen contents (Fasted-Evac). The plasma variables measured did not differ (P>0.10) between Fasted and Fasted-Evac cows. Plasma leptin, insulin, and IGF-1 concentrations were reduced by 10, 6, and 24h of fasting, respectively, in Fasted-Evac cows; and these variables were reduced by 24h in Fasted cows (P<0.05). Plasma glucose levels were reduced (P<0.05) by 48 h of fasting in both groups of fasted animals. Plasma NEFA and GH levels were increased (P<0.05) by 12 and 48 h of fasting, respectively. In experiment 3, postpubertal Holstein heifers were either fed ad libitum (Control, n=4) or feed deprived for 72 h (Fasted, n=5). Concentrations of leptin, insulin, IGF-1, and glucose in plasma were reduced (P<0.05) by 24, 10, 24, and 48 h of fasting, respectively. Plasma NEFA concentrations increased (P<0.05) by 4h, of fasting while GH levels were not significantly (P>0.10) affected by fasting. Collectively, our data provide evidence that plasma leptin concentrations are reduced with short-term fasting and rebound on refeeding in dairy cattle with the response dependent on the physiological state of the animals. Compared to the rapid induction of hypoleptinemia with fasting of early lactation cows, the fasting-induced hypoleptinemia was delayed in non-lactating cows and postpubertal heifers.

Animals↗
PubMed1993

Suppression of luteinizing hormone secretion during short-term fasting in male rhesus monkeys: the role of metabolic versus stress signals.

One day of fasting leads to a significant suppression of pulsatile LH secretion in adult male rhesus monkeys that is evident within the first 4-6 h after a missed meal. Restricting food intake may suppress the central drive to the reproductive axis via metabolic signals occurring during the transition from a fed, energy storing state to a fasted, energy mobilizing state or via signals associated with the "psychological stress" imposed by withholding food. To distinguish between these two general types of signals, we chose the experimental strategy of providing monkeys with a great excess of calories on the day before fasting (i.e. overfeeding on the day before fasting) in order to maintain them in a metabolically fed state on the following day when they were fasted, without preventing the psychological stress associated with fasting. We reasoned that if metabolic signals are responsible for causing the fasting-induced suppression of LH secretion, overfeeding on the day before fasting would prevent the fasting-induced suppression of LH secretion. Eight adult male rhesus monkeys with indwelling venous catheters were studied on three occasions: on a day of normal feeding (receiving approximately 30 pellets of monkey chow at 1100 h on the day of the study), on a day of fasting after a day of normal feeding, and on a day of fasting after a day of overfeeding (receiving one meal of 100 pellets on the day before the study). Pulsatile LH secretion on a day of fasting after a day of normal feeding (0.4 +/- 0.2 pulses/6 h, measured from 1200-1800 h) was significantly suppressed, P < 0.05, compared to a day of normal feeding (1.8 +/- 0.3 pulses/6 h). In contrast, on a day of fasting after a day of overfeeding there was no significant difference in LH secretion measured from 1200-1800 h (1.5 +/- 0.3 pulses/6 h) compared to a day of normal feeding. Overfeeding the day before fasting prevented the normal fasting-induced suppression of plasma T3 concentrations and delayed the normal fasting-induced decline in plasma insulin concentrations. Overfeeding did not prevent the display of agitated behavior that we have previously documented in monkeys when they are fasted. These results support the hypothesis that the signal(s) which suppresses normal LH secretion after brief periods of fasting is related to the metabolic status of the body during the transition from a fed to a fasted state, rather than a function of the psychological state imposed by withholding food.

Animals↗
PubMed1996

Fasting as a metabolic stress paradigm selectively amplifies cortisol secretory burst mass and delays the time of maximal nyctohemeral cortisol concentrations in healthy men.

Serum cortisol concentrations are increased in fasted or malnourished human subjects. The dynamic mechanisms underlying this adaptive response have been investigated in eight normal men by analyzing serum cortisol concentrations measured in blood obtained at 5-min intervals over 24 h on a control (fed) day and on the fifth day of a fast (water only) assigned in randomized order. A multiple parameter deconvolution method was used to simultaneously resolve endogenous cortisol secretion and half-life. Five days of fasting induced a 1.8-fold increase in the 24-h endogenous cortisol production rate (fed, 2504 +/- 308; fasted, 4528 +/- 488 nmol/L distribution volume; P < 0.006). This enhanced cortisol production rate was accounted for by a 1.6-fold increase in the mass of cortisol secreted per burst (fed, 115 +/- 12.1; fasted, 183 +/- 17.3 nmol/L; P < 0.02). Cortisol secretory event amplitudes (maximal rates of cortisol release attained within a burst) increased in seven of eight men, and mean secretory burst durations remained unchanged by fasting. Moreover, the number of computer-resolved cortisol secretory bursts per 24 h (fed, 22 +/- 1.4; fasted, 25 +/- 2.0; P = NS) and the interburst interval (fed, 65 +/- 4.0; fasted, 57 +/- 4.4 min) did not change significantly during a 5-day fast. The calculated half-life of endogenous cortisol was not significantly altered by fasting (fed, 108 +/- 9.7; fasted, 129 +/- 11 min). There was no significant change in the nyctohemeral pattern of varying adrenocortical secretory burst frequency in response to fasting. However, the mean (mesor) mass of glucocorticoid secreted per burst over 24 h rose significantly in response to fasting. In addition, by cosinor analysis, maximal serum cortisol concentrations occurred (95% confidence intervals) between 0930-1334 h in the fed state and between 1116-1612 h in the fasted state (P < 0.04). Fasting augmented the mesor (average value about which the diurnal rhythm oscillates; P < 0.0008 compared with fed state) and the amplitude (P < 0.04) of the 24-h serum cortisol concentration profile. Linear regression analysis disclosed a significant inverse relationship between mean serum cortisol and GH concentrations in fasted men (r = -0.76; P < 0.02). In conclusion, the present data indicate that starvation-induced enhancement of cortisol secretion in young healthy men is mediated by an increased glucocorticoid secretory burst mass, rather than changes in secretory burst frequency or duration or in cortisol half-life. In addition, fasting modifies the diurnal secretory pattern of cortisol by delaying maximal serum concentrations to the early afternoon. The inverse relationship between serum cortisol and GH responses to fasting suggests differential regulation of the corticotropic and somatotropic axis by the metabolic stress of fasting and/or feedback interactions between these two axes when they are both activated.

Adult↗
PubMed1999

White matter lesion contrast in fast spin-echo fluid-attenuated inversion recovery imaging: effect of varying effective echo time and echo train length.

OBJECTIVE: Our aim was to determine whether the contrast between white matter lesions and normal-appearing white matter in fast spin-echo fluid-attenuated inversion recovery (FLAIR) images can be improved by lengthening the effective TE and the echo train length. SUBJECTS AND METHODS: Thirty patients with various white matter lesions were imaged using fast spin-echo FLAIR sequences (TR = 10,002 msec; inversion time = 2200) on a 1.5-T MR imaging system. For 14 patients, fast spin-echo FLAIR sequences with a TE of 165 msec and echo train length of 32 (fast spin-echo FLAIR 165/32) were compared with fast spin-echo FLAIR sequences with a TE of 125 msec and echo train length of 24 (fast spin-echo FLAIR 125/24). For 16 other patients, fast spin-echo FLAIR 165/32 sequences were compared with fast spin-echo FLAIR sequences with a TE of 145 msec and echo train length of 28 (fast spin-echo FLAIR 145/28). Signal difference-to-noise ratios were calculated between the lesions and normal-appearing white matter for a typical lesion in each patient. RESULTS: In both groups, a small but statistically significant increase in the signal difference-to-noise ratio was found on the fast spin-echo FLAIR sequences using the longer TE and echo train length. In the first group, signal difference-to-noise ratio increased from 18.7 +/- 4.7 (mean +/- SD) for fast spin-echo FLAIR 125/24 to 20.1 +/- 4.5 for fast spin-echo FLAIR 165/32 (p < .05). In the second group, the signal difference-to-noise ratio increased from 15.4 +/- 4.0 for fast spin-echo FLAIR 145/28 to 16.8 +/- 4.6 for fast spin-echo FLAIR 165/32 (p <.01). In addition, fast spin-echo FLAIR sequences with a longer TE and echo train length were obtained more rapidly (6 min for fast spin-echo FLAIR 125/24, 5 min 20 sec for fast spin-echo FLAIR 145/28, and 4 min 41 sec for fast spin-echo FLAIR 165/32). CONCLUSION: Lengthening the TE to 165 msec and echo train length to 32 in fast spin-echo FLAIR imaging allows both a mild improvement in the contrast between white matter lesions and normal-appearing white matter and shorter imaging times.

Brain↗
PubMed1998

The effect of short-term fasting, phenobarbital and refeeding on apoptotic loss, cell replication and gene expression in rat liver during the promotion stage.

Previous work from this laboratory has reported on the effects of two sequential 5 day periods of fasting and subsequent refeeding on tumor promotion in multistage hepatocarcinogenesis in the rat (Carcinogenesis, 18, 159-166, 1997). In the present extension of the earlier study, the sequential fasting-refeeding regimen was begun at later time points (28 and 54 days post-initiation) than the first study. This was done to determine whether larger-sized altered hepatic foci (AHF) exhibited a depletion similar to that of the relatively small AHF in the published experiment and to study concomitant molecular changes during the fasting periods. Groups of animals were fasted in the presence and absence of 0.05% phenobarbital (PB) in the drinking water. During the fasting periods, both body and liver weights decreased dramatically, less in the fast begun at 54 days. This change was accompanied by a significant decrease in the bromodeoxyuridine (BrdU) labeling indices of hepatocytes within AHF. Apoptotic bodies increased dramatically in the non-focal (surrounding the AHF) hepatocytes during the fasting periods. These parameters were slightly lower in hepatocytes of rats administered PB during the fasting periods, most notably during the 54-66 day period. With the nick end-labeling method, the proportion of hepatocytes undergoing apoptosis was significantly higher in cells within AHF at the end of each of the fasting periods in all but one group. Concomitantly, the number of AHF and percentage of liver volume occupied by AHF decreased dramatically during the fasting periods. Refeeding caused a marked increase in BrdU labeling in hepatocytes within and surrounding AHF during the first week or two, most notably in animals not receiving PB during the fasting period. Both the number and volume percentage of liver AHF returned to control values within approximately 2 weeks of the refeeding regimen. Assays of nuclear DNA fragmentation with samples of whole liver indicated that a 'laddering' effect was most noticeable in livers of animals subjected to the fasting-refeeding regimen when phenobarbital was not present during the fasting period. Studies of the levels of mRNA of several genes in the total liver revealed that the expression of c-myc increased 3- to 9-fold during the fasting periods but rapidly returned to normal levels after refeeding. Levels of albumin and insulin-like growth factor I mRNAs decreased significantly during the fasting period, but rapidly reappeared on refeeding. These results indicate that the extensive loss of AHF during the short-term fasting periods occurs even when the number and volume of AHF are 10- to 50-fold greater at the beginning of the fast than the values published previously. Both the decrease in insulin growth factor I and the elevation of c-myc expression during the fasting period may indicate the role of these genes in the transcriptional regulation of hepatocyte apoptosis in both normal and preneoplastic hepatocytes in the rat.

Actins↗
PubMed2000

Neuroendocrine consequences of fasting in adult male macaques: effects of recombinant rhesus macaque leptin infusion.

Fasting inhibits the gonadotropic axis and stimulates the corticotropic and somatotropic axes. Since leptin is a product of fat cells that has been implicated in the control of both reproduction and metabolism, we hypothesized that the decrease in leptin observed during fasting was responsible for these effects on reproductive and metabolic hormones. Recombinant rhesus leptin (rrhLep) produced in our laboratory was infused (100 microgram/h) into fasted adult male rhesus macaques (6-9 kg) beginning at midnight after the first missed meal and continuing until the end of the study. Bioactive luteinizing hormone (LH), testosterone, cortisol and growth hormone (GH) were measured in plasma from samples collected at 15-min intervals for the last 15 h (42-57 h) of the fast. We analyzed pulsatile LH and GH secretion by deconvolution analysis and the orderliness of pulsatile LH and GH release by the approximate entropy (ApEn) statistic. There was no difference in LH pulse frequency between control and fasted groups, but there was a significant decrease in the mean concentration of LH released (7.6 +/- 1.4 ng/ml control vs. 2.7 +/- 0.65 ng/ml fasted) that was not relieved with rrhLep infusions (2.8 +/- 0.83 ng/ml). Model-free Cluster analysis confirmed these inferences and also indicated that the peak height was lower in the fasted (4.6 +/- 1.0 ng/ml) and the fasted + rrhLep (2.85 +/- 1.0 ng/ml) groups compared to controls (16. 3 +/- 1.4 ng/ml). Testosterone levels reflected those of LH. Fasting resulted in an increase in GH secretory pulse frequency (5.3 +/- 0. 95 pulses/15 h control vs. 12.8 +/- 1.4 pulses/15 h fasted) and this increase was not affected by rrhLep infusion (12.5 +/- 1.4 pulses/15 h). In addition, fasting also increased the ApEn (decreased the orderliness) of pulsatile GH secretion, and this characteristic was not relieved with rrhLep infusions. Cortisol levels in fasted animals were 2- to 3-fold higher than those observed in control studies, and this increase was particularly pronounced at the time when the animals expected their first meal of the day. The increase in circulating cortisol observed in fasted animals was not affected by rrhLep infusion. Glucose levels at the end of the sampling period were 80 mg/dl in controls, 48 mg/dl in fasted animals and 58 mg/dl in the fasted + rrhLep group. Circulating leptin levels averaged 1.2 +/- 0.37 ng/ml in control animals, 0.7 +/- 0.2 ng/ml in fasted animals and 10.1 +/- 5.6 ng/ml in fasted animals infused with rrhLep. These studies suggest that intravenous replacement with homologous leptin does not reverse the acute changes in GH, LH and cortisol secretion observed with fasting in the adult male macaque.

Animals↗
PubMed1998

Fasting suppresses pulsatile luteinizing hormone (LH) secretion and enhances orderliness of LH release in young but not older men.

Pulsatile gonadotropin secretion and sex-steroid concentrations are suppressed reversibly in young fasted or malnourished human subjects. In this study, we investigated the impact of age on the dynamic neuroendocrine mechanisms underlying this stress response in healthy young (age, 28 +/- 3 yr, n = 8) vs. older (age 67 +/- 2 yr, n = 8) men with similar body mass indices (mean, 26 +/- 0.6 vs. 26 +/- 1.3 kg/m2, respectively). Serum LH concentrations were measured by immunoradiometric assay (IRMA) in blood collected at 10-min intervals over 27 h on a control (fed) day and on the third day of a 3.5-day fast (water only) assigned in randomized order. After 24 h of basal sampling, GnRH (10 micrograms i.v. bolus) was administered to test gonadotrope responsiveness. Cortisol, dehydroepiandrosterone sulfate, androstenedione, testosterone, FSH, GH, and PRL were measured in 24-h pooled serum as positive and negative control hormones. Approximate entropy was used to quantitate the orderliness of LH release over 24 h, and a multiple-parameter deconvolution method was applied to quantify pulsatile LH secretion and LH half-life. In the fed state, older men exhibited elevated mean (24-h pooled) serum FSH and cortisol concentrations compared with young controls but equivalent serum LH concentrations and reduced serum GH, free testosterone, androstenedione, and dehydroepiandrosterone sulfate concentrations. Fed older men also manifested a lower frequency and amplitude of 24-h pulsatile LH secretion, and, by approximate entropy calculations, a more disorderly pattern of basal LH release than younger individuals. Three- and one-half days of fasting evoked 40% and 47% increases in mean (24-h) serum cortisol concentrations in young and older men, respectively (P < 0.01 vs. fed, but P = not significant for percentage rise in older vs. young men). Concurrently, fasting induced a 2.1-fold fall in the 24-h endogenous LH production rate in young men (fed 36 +/- 9.7 vs. fasted 17 +/- 2.0 IU/L of distribution volume/day, P < 0.01), but did not significantly affect the daily LH secretion rate in older men (fed 27 +/- 4.5 vs. fasted 21 +/- 3.4 IU/day). The reduced LH production rate in fasting young men was accounted for by a 1.7-fold decline in the mass of LH secreted per burst (fed 2.5 +/- 0.45 vs. fasted 1.5 +/- 0.16 IU/L, P < 0.05), whereas LH burst mass in older men remained unchanged (and low) during fasting. In addition, in young men, during the 3.5-day fast the number of computer-resolved LH secretory bursts per 24 h decreased (fed 15 +/- 0.7 vs. fasted 11 +/- 0.7, P < 0.01), and the interburst interval increased (fed 94 +/- 4.2 vs. fasted 125 +/- 8.7 min, P < 0.05). In contrast, in older men in the fed state, basal LH peak frequency and serum free testosterone concentrations were reduced compared with corresponding values in young men, and did not decline further with fasting. Whereas the orderliness of LH release patterns increased significantly during fasting in the young men, the approximate entropy measure failed to change significantly in unfed older subjects. By cosinor analysis, young men showed lower 24-h mesor (mean of nyctohemeral rhythm of) serum LH concentrations than older volunteers during fasting. Moreover, young but not older men manifested preserved 24-h variations in LH interpulse intervals when fasting. Exogenously stimulated LH release (mean 3-h serum LH concentration or calculated mass of LH secreted) following a single i.v. injection of 10 micrograms GnRH was independent of age and fasting status. We conclude that the metabolic stressor of short-term fasting unmasks specific age-related neuroendocrine contrasts in the stress-responsive control of both the pulsatile and nyctohemeral regulation of the male hypothalamo-pituitary-gonadal-axis.

Adult↗
PubMed1989

Fast hyperpolarization following an excitatory postsynaptic potential in cat bladder parasympathetic neurons.

Intracellular recording techniques were used to study a fast hyperpolarizing potential following the fast excitatory postsynaptic potential evoked by an orthodromic nerve stimulation in cat bladder parasympathetic ganglion cells. In the 61 ganglion cells examined, two types of responses were recorded on stimulating the preganglionic nerve; one had only a fast excitatory postsynaptic potential (type SI, n = 20) and the other had a fast excitatory postsynaptic potential followed by a fast hyperpolarizing potential (type SII, n = 41). In type SII neurons, the half-maximum duration of the afterhyperpolarizing potential following an orthodromic spike was longer than that of a direct spike produced by injecting a depolarizing current pulse through the recording electrode; the half-maximum durations for afterhyperpolarizing potentials following orthodromic and direct action potentials were comparable in type SI cells. Blocking the initiation of an orthodromic spike by hyperpolarizing the membrane in type SII cells revealed a fast excitatory postsynaptic potential followed by a fast hyperpolarizing potential which was similar to that observed at the resting potential. The fast hyperpolarizing potential had a duration comparable to that of an afterhyperpolarizing potential following an orthodromic action potential. The fast excitatory postsynaptic potential-fast hyperpolarizing potential sequence was blocked completely and reversibly by nicotinic receptor antagonists (hexamethonium and D-tubocurarine). Atropine, alpha-2 noradrenergic (yohimbine and phentolamine), and purinergic (caffeine) antagonists had no effect on the fast hyperpolarizing potential. In cells which show type SII responses, spontaneous excitatory postsynaptic potentials were not followed by a hyperpolarization. Depolarizing the membrane (by passing a cathodal current through the recording electrode) to an amplitude comparable to that of a fast excitatory postsynaptic potential also did not elicit a membrane hyperpolarization in type SII cells. In some cells, stimulating one preganglionic nerve trunk elicited a fast hyperpolarizing potential, but activating another nerve trunk innervating the same ganglion cell did not. There was no correlation between the variations in the amplitudes of the fast excitatory postsynaptic potential and the fast hyperpolarizing potential in type SII cells, but increasing the stimulus intensity applied to the presynaptic nerve fiber potentiated the amplitude of the fast excitatory postsynaptic potential and the fast hyperpolarizing potential. The fast hyperpolarizing potential was not associated with appreciable changes in input resistance.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1993

The regulation of insulin-like growth factor binding protein (IGFBP)-1 during prolonged fasting.

OBJECTIVE: Insulin-like growth factor binding protein (IGFBP)-1 levels increase overnight, being inversely related to changes in insulin. With prolonged fasting IGFBP-1 levels increase further. In animal studies high IGFBP-1 levels increase plasma glucose levels possibly by regulating the insulin-like actions of 'bio-available' plasma IGF. Following prolonged fasting, there is an increase in insulin requirement. A proportion of this reversible insulin resistance may be due to inhibitory effects of high IGFBP-1 levels on IGF action. This study examined the regulation of IGFBP-1 in the presence of reversible insulin resistance. SUBJECTS: Nine normal adult volunteers, seven female and two male (mean age 27.6 +/- SD 2.6 years, range 21.7-46.0 years) of normal body mass index were studied. METHODS: Subjects fasted from 2200 h day 0 to 0900 h day 3 (59 hours), the fast being completed with a 75-g glucose meal. At least one week later, an 11-hour overnight fast was performed, followed by a repeat glucose meal. Blood samples were taken at regular intervals from 0900 h day 1 and for 5 hours during both glucose meal studies via an indwelling cannula. MEASUREMENTS: Serum levels of IGFBP-1, insulin, GH, glucose, IGF-I and cortisol were measured at varying intervals during the fast and both glucose meal studies. RESULTS: Following the initial 11-hour overnight fast IGFBP-1 levels rose from (mean +/- SEM) 32 +/- 5 micrograms/l to reach a maximum of 144 +/- 24 micrograms/l after 32 hours of fasting. IGFBP-1 levels then fluctuated, falling in the morning (93 +/- 8 micrograms/l) and then rising overnight (126 +/- 9 micrograms/l), but not regaining the initial peak levels. The increase of IGFBP-1 from overnight fasting levels was associated with a fall in plasma insulin from 5.7 +/- 0.7 to 2.2 +/- 0.2 mU/l. In comparison, 30 minutes after termination of the fast with the glucose meal, IGFBP-1 levels fell from 120 +/- 11 to 24 +/- 2 micrograms/l within 4 hours. After an overnight fast IGFBP-1 levels fell from 35 +/- 5 to 13 +/- 2 micrograms/l within 3 hours. There was glucose intolerance and increased insulin levels following the glucose meal preceded by the 59-hour fast when compared with the overnight fast. The fall of IGFBP-1 levels after the glucose meal was best expressed, taking into account subject variation, by the following regression equations: Glucose meal preceded by 11-hour fast: log [IGFBP-1] = 1.64-0.255 log [1 h previous insulin] (R2 0.51); Glucose meal preceded by 59-hour fast: log [IGFBP-1] = 1.41-0.265 log [1 h previous insulin] + 0.557 log [current glucose] (R2 0.82). CONCLUSION: In man, insulin appears to regulate circulating IGFBP-1 levels in all circumstances, this regulation being unaffected by the resistance to insulin action induced by prolonged fasting. The high IGFBP-1 levels were statistically related to the higher glucose levels and may have directly contributed to the increased insulin requirement observed after prolonged fasting.

Adult↗
PubMed2006

The electrophysiological characteristics in patients with ventricular stimulation inducible fast-slow form atrioventricular nodal reentrant tachycardia.

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) can usually be induced by atrial stimulation. However, it seldom may be induced with only ventricular stimulation, especially the fast-slow form of AVNRT. The purpose of this retrospective study was to investigate the specific electrophysiological characteristics in patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation. METHODS: The total population consisted of 1,497 patients associated with AVNRT, and 106 (8.4%) of them had the fast-slow form of AVNRT and 1,373 (91.7%) the slow-fast form of AVNRT. In patients with the fast-slow form of AVNRT, the AVNRT could be induced with only ventricular stimulation in 16 patients, Group 1; with only atrial stimulation or both atrial and ventricular stimulation in 90 patients, Group 2; and with only atrial stimulation in 13 patients, Group 3. We also divided these patients with slow-fast form AVNRT (n = 1,373) into two groups: those that could be induced only by ventricular stimulation (Group 4; n = 45, 3%) and those that could be induced by atrial stimulation only or by both atrial and ventricular stimulation (n = 1.328, 97%). RESULTS: Patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation had a lower incidence of an antegrade dual AVN physiology (0% vs 71.1% and 92%, P < 0.001), a lower incidence of multiple form AVNRT (31% vs 69% and 85%, P = 0.009), and a more significant retrograde functional refractory period (FRP) difference (99 +/- 102 vs 30 +/- 57 ms, P < 0.001) than those that could be induced with only atrial stimulation or both atrial and ventricular stimulation. The occurrence of tachycardia stimulated with only ventricular stimulation was more frequently demonstrated in patients with the fast-slow form of AVNRT than in those with the slow-fast form of AVNRT (15% vs 3%, P < 0.001). Patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation had a higher incidence of retrograde dual AVN physiology (75% vs 4%, P < 0.001), a longer pacing cycle length of retrograde 1:1 fast and slow pathway conduction (475 +/- 63 ms vs 366 +/- 64 ms, P < 0.001; 449 +/- 138 ms vs 370 +/- 85 ms, P = 0.009), a longer retrograde effective refractory period of the fast pathway (360 +/- 124 ms vs 285 +/- 62 ms, P = 0.003), and a longer retrograde FRP of the fast and slow pathway (428 +/- 85 ms vs 362 +/- 47 ms, P < 0.001 and 522 +/- 106 vs 456 +/- 97 ms, P = 0.026) than those with the slow-fast form of AVNRT that could be induced with only ventricular stimulation. CONCLUSION: This study demonstrated that patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation had a different incidence of the antegrade and retrograde dual AVN physiology and the specific electrophysiological characteristics. The mechanism of the AVNRT stimulated only with ventricular stimulation was supposed to be different in patients with the slow-fast and fast-slow forms of AVNRT.

Adolescent↗
PubMed1989

Interaction of platinum(II) tetrachlorodianion (Fast Black)2 with superhelical DNA and with radiation in vitro and in vivo.

A new complex of tetrachloroplatinum(II) and the azoic diazo dye, Fast Black K, Pt(Fast Black)2, was made in an attempt to produce an uncharged molecule which could readily gain access into cells and could bring a high concentration of tetrachloroplatinum into the vicinity of the DNA. Even the lowest concentration of Pt(Fast Black)2 tested in the superhelical pBR322 plasmid DNA assay in vitro completely converted the superhelical DNA to the circular and linear forms by 24 h. When the cytotoxicity of the Pt(Fast Black)2 and Fast Black were tested in exponentially growing EMT6 cells. Pt(Fast Black)2 was slightly more toxic to normally oxygenated than to hypoxic cells at pH 7.40, but was far more toxic to cells at pH 6.45 with no difference based on cellular oxygenation. Fast Black was much less toxic than Pt(Fast Black)2 and its cytotoxicity was unaffected by pH. Pt(Fast Black)2 had a small radiosensitizing effect on hypoxic EMT6 cells with a dose-modifying factor of 1.3, but exposure to the drug entirely removed the shoulder region on the radiation survival curves for both the oxygenated and hypoxic cells. In contrast, Fast Black reduced the shoulder in hypoxic but not in oxygenated cells. When Pt(Fast Black)2 (500 mg/kg), Fast Black (300 mg/kg) (the maximally tolerated dose), or misonidazole (1 g/kg) were given intraperitoneally 15 min prior to irradiation of FSaIIC tumors with 0, 10, 20, or 30 Gy, Pt(Fast Black)2 alone caused a tumor growth delay of 6 days versus 3 days for Fast Black. With radiation, Pt(Fast Black)2 produced the greatest enhancement in tumor growth delay of the drugs tested, especially at the lowest (10 Gy) radiation dose (i.e., in the in vivo "shoulder region"). These results indicate that Pt(Fast Black)2 may be suitable for clinical development because it causes both significant direct cytotoxicity and enhancement of radiation killing. The fact that its cytotoxicity is markedly increased at an acidic pH and its radiation enhancing effects are greatest in combination with relatively low single-fraction radiation doses make it especially interesting. The cytotoxicity of Pt(Fast Black)2 may be influenced by the tumor environment, and the radiosensitizing properties appear well suited for use with radiation fraction sizes that are employed in the clinic.

Animals↗
PubMed2005

The influence of short-term fasting on the quality of small bowel graft preservation.

INTRODUCTION: Donor nutritional status may be a determinant of small bowel (SB) quality following storage. In this study, we investigated the effect of donor nutritional status and a proven nutrient-rich preservation solution on graft quality following cold storage. METHODS: Rats were fasted (12-14 h) or non-fasted. SB (n=6) was flushed vascularly with modified University of Wisconsin (UW) solution and flushed luminally with UW or an amino acid-rich (AA) solution as follows: Fasted. UWV, none; UWL, UW solution; AAL, AA solution. Non-fasted. UWV, none; UWL, UW solution; AAL, AA solution. Energetics, peroxidation (malondialdehyde; MDA), glutathione and histology were assessed over 24 h at 4 degrees C. RESULTS: Energetics (ATP, ATP/ADP, and energy charge) were significantly higher in AAL (fasted and non-fasted) groups than other groups. However, there were no differences in energetics parameters between fasted and non-fasted animals in all groups. MDA was higher in fasted groups than non-fasted tissues; interestingly, AAL values were up to 10-fold lower than other groups. Higher glutathione levels were detected in non-fasted AAL tissues. Mucosal integrity was markedly superior in luminally treated tissues (UWL and AAL) in fasted and non-fasted states. Most noteably, AAL tissues from fasted animals exhibited grade 2 injury (villus clefting), whereas normal mucosa was observed in non-fasted tissues (grade 0). CONCLUSION: Luminal flushing and a nutrient-rich preservation solution improve energetics, oxidative stress, and mucosal integrity during storage. Poorer donor nutritional status does not affect energetics throughout storage, but causes mucosal injury as a result of increased oxidative stress, even after a brief period of donor fasting.

Adenosine↗
PubMed2001

Acute stimulation of leptin concentrations in humans during hyperglycemic hyperinsulinemia. Influence of free fatty acids and fasting.

OBJECTIVE: To assess the acute regulation of leptin concentrations by insulin, glucose and free fatty acids (FFAs). DESIGN: Four protocols: saline control experiment (CON); hyperglycemic clamps (approximately 8.3 mmol/l, 120 min) after an overnight fast (12 FAST); after a 36 h fast (36 FAST); and after a 36 h fast during which Intralipid/heparin was given over the last 24 h (36 FAST+FFA). SUBJECTS: Lean, young, healthy volunteers; control group (n=6), experimental group (n=6). MEASUREMENTS: Serum leptin concentrations. RESULTS: Glucose and insulin concentrations were similar during the three clamp protocols. Average FFAs during the last 60 min of the clamp were 671+/-68 microM (CON),109+/-15 microM (12 FAST), 484+/-97 microM (36 FAST) and 1762+/-213 microM (36 FAST+FFA). Leptin concentrations decreased similarly during 36 FAST and 36 FAST+FFA. Leptin concentrations at 120 min (expressed as percentage of mean basal value) were 0.82+/-0.02 (CON), 0.93+/-0.08 (12 FAST) (P=0.29), 1.19+/-0.06 (36 FAST) (P<0.01) and 1.44+/-0.12 (36 FAST+FFA) (P<0.01). CONCLUSION: During a one-day fast leptin concentrations decrease regardless of maintainance of an isocaloric balance. During acute hyperinsulinemic hyperglycemia leptin concentrations increase only after a preceding fast. This increase was most pronounced during simultaneous elevation of FFAs. Overall, our findings are compatible with the hypothesis that leptin secretion may be coupled to triglyceride synthesis rather than to the absolute lipid content of the adipocyte. International Journal of Obesity (2001) 25, 138-142

Adult↗