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 901 records · Page 50Linked to original sources

Short-term fasting affects locomotor activity, corticosterone, and corticosterone binding globulin in a migratory songbird.

Unpredictable events such as severe storms lead to an increase in circulating corticosterone (CORT) in breeding birds. This increase is often accompanied by elevations in foraging and irruptive behavior. We were interested in determining if acute food restriction (such as might occur during inclement weather) is a sufficient cue to elicit an increase in locomotor activity, increase CORT secretion, and/or decrease circulating levels of corticosterone binding globulin (CBG) in white-crowned sparrows (Zonotrichia leucophrys gambelii). Male Z.l. gambelii were housed individually in environmental chambers on long days (LD 20:4) to simulate breeding season daylength. Birds were fed ad libitum, and on select days, food was removed 2 h after lights on (fasted treatment), or was removed and replaced (control). We analyzed CORT and CBG levels after 1, 2, 6, 22 (lights on), and 23 h under fasted and control conditions. We also measured activity during the 23-h experiment. Activity levels were increased under fasted conditions during the daytime relative to control conditions, but activity levels did not differ between treatments during the night. Fasting as little as 1, 2, and 6 h significantly increased total CORT levels above baseline (control), although after 22 h, total CORT levels under fasted conditions matched those under control conditions. Plasma CBG decreased after the 22-h fast, and remained low after the 23-h fast. This change was sufficient to significantly elevate free CORT levels in fasted birds relative to ad libitum food conditions, despite the lack of difference in total CORT levels.

Animal Migration↗

Sedation in children: adequacy of two-hour fasting.

OBJECTIVES: (1) To investigate the relationship between the duration of time that children fasted before a procedure and their gastric volume and pH at the time of the procedure. (2) To compare the variables of gastric pH and volume with historical standards. METHODS: We performed 285 gastroscopies for children aged 0.1 to 18.6 years (mean, 7.5 +/- 5.3) between October 1991 and January 1995. Duration of fasting was 0.5 to 24 hours (mean, 6.7 +/- 5.3) after ingestion of clear liquids. Immediately after intravenously administered sedation, the gastric contents were removed endoscopically with suction and direct visualization to ensure complete evacuation. The volume and pH of the gastric contents were measured and analyzed in comparison with the duration of fasting. The values obtained were also compared with historical standards thought to minimize the risk of aspiration pneumonia: gastric volume 0.4 ml or less per kilogram of body weight and pH of 2.5 or greater. RESULTS: There was no significant correlation between duration of fasting and either gastric volume divided by body weight (mean, 0.68 +/- 1.31 ml/kg; range, 0 to 15.23 ml/kg) or pH (mean, 2.03 +/- 1.40; range, 1 to 8). There was less no significant difference in the percentage of children with gastric volume of 0.4 ml/kg or less or with pH of 2.5 or greater between the groups with the following fasting times: 30 minutes to 3 hours, more than 3 hours to 8 hours, and more than 8 hours. CONCLUSIONS: On the basis of the data in this study and a review of the literature, we concluded that (1) fasting longer than 2 hours after ingesting clear liquids does not significantly change gastric volume or pH, (2) there is no advantage in requiring children to fast for longer than 2 hours after clear liquid ingestion before sedation or anesthesia for any procedure, and (3) fewer than half of pediatric patients actually achieve the "desirable" values of a gastric volume of 0.4 ml/kg or less and a pH value of 2.5 pH units or more, regardless of fast duration, even though these values are presented in the literature as a goal to minimize the risk of aspiration pneumonia.

Adolescent↗

Fasting increases gene expressions of uncoupling proteins and peroxisome proliferator-activated receptor-gamma in brown adipose tissue of ventromedial hypothalamus-lesioned rats.

Uncoupling proteins (UCPs) are supposed to be involved in diet-induced thermogenesis. Their activities are usually elevated by feeding and reduced by fasting in normal animals. To investigate whether fasting affects the expression of UCPs mRNA in brown adipose tissue (BAT) of bilateral ventromedial hypothalamus (VMH)-lesioned rats, we determined the gene expression of UCP1, UCP2 or UCP3 in BAT of VMH-lesioned rats and examined oxygen consumption in these rats under fed or 48-h fasted conditions. Northern blotting revealed no difference in the expression of UCPs mRNA in BAT between VMH-lesioned and sham-operated rats under the fed condition, however, expressions were increased markedly in BAT of VMH-lesioned rats under the fasted condition. Under the fed condition, no difference in oxygen consumption was observed between VMH-lesioned and sham-operated rats. Under the fasted condition, oxygen consumption decreased in both rats, however, it decreased in VMH-lesioned less than in sham operated rats. To explore the mechanism that fasting elevated BAT UCPs mRNA in VMH-lesioned rats, we measured peroxisome proliferator-activated receptor (PPAR)-gamma mRNA and protein in BAT, because PPAR-gamma agonist can elevate UCPs mRNA levels in BAT. Under the fed condition, no differences in the expression of PPAR-gamma mRNA and protein content were observed between in BAT of VMH-lesioned and sham-operated rats. Under the fasted condition, however, both increased in BAT of VMH-lesioned rats. These results suggest that VMH-lesions enhance the gene expression of UCPs in BAT under long-term fasting as a defensive reaction to inhibit the reduction of body temperature through an increase in PPAR-gamma activity.

Adipose Tissue, Brown↗

No evidence of linkage between the very-low-density lipoprotein receptor gene and fasting serum insulin or homeostasis model assessment insulin resistance index: the National Heart, Lung, and Blood Institute Family Heart Study.

A major gene effect on the fasting insulin level and insulin resistance has been suggested in previous studies. Several candidate genes for insulin resistance in rare syndromes have been proposed. However, there has been limited success in finding genes for common forms of insulin resistance. There is accumulating evidence of a relationship between insulin resistance and a disturbance of free fatty acid (FFA) metabolism. The very-low-density lipoprotein (VLDL) receptor, which is associated with FFA metabolism, could serve as a possible candidate gene for insulin resistance. We performed linkage analyses between the VLDL receptor gene and fasting insulin and the homeostasis model assessment (HOMA) insulin resistance index (fasting insulin x fasting glucose/22.5) in 1,050 sibpairs participating in the phase II physical examination of the National Heart, Lung, and Blood Institute Family Heart Study (FHS). Data analyses were completed using the SIBPAL component of the SAGE software package (SAGE, Statistical Analysis for Genetic Epidemiology, Version 3.1; Computer program package available from the Department of Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, OH, 1997). We did not find evidence for linkage of the fasting insulin or the HOMA insulin resistance index with a polymorphic marker at the VLDL locus (P = .316 and .402, respectively). Adjustment of fasting insulin and the HOMA insulin resistance index for the body mass index (BMI) did not change the results (P = .319 and .472, respectively). In conclusion, no evidence was found for a linkage between a locus controlling the fasting insulin level or HOMA insulin resistance index and a VLDL polymorphism in the present study. Additional adjustment of fasting insulin or the HOMA insulin resistance index for the BMI did not change the linkage results significantly.

Blood Glucose↗

Developmental plasticity in sympathetic nervous system response to fasting in adipose tissues of male rats.

While fasting suppresses sympathetic nervous system (SNS) activity in most peripheral tissues, the response of sympathetic nerves in white adipose tissue (WAT) is reportedly stimulatory. To confirm this finding and to determine if the fasting response in WAT is susceptible to developmental modification, SNS activity was compared in fed and fasted animals using techniques of [3H]norepinephrine ([3H]NE) turnover. Studies were performed in commercially reared 7-week-old male rats, in male rats reared in the local vivarium, and in male rats reared until 30 days of age at either 18 degrees C or 30 degrees C. In commercially reared animals, [3H]NE turnover was elevated in epididymal fat during the second day of fasting, a response not seen during the preceding or succeeding day of fasting. On the other hand, in rats reared from birth in the local vivarium a 1-day fast led to suppression of SNS activity in epididymal fat. In rats reared at 18 degrees C for the first 30 days of life, fasting suppressed SNS activity in retroperitoneal fat in contrast to the absence of this response noted in 30 degrees C-reared rats. These studies demonstrate that sympathetic responses in WAT to fasting in young adult, male rats are susceptible to modification by the environmental conditions present during the first month of life.

Adipose Tissue↗

Relationships between fasting plasma insulin, anthropometrics, and metabolic parameters in a very old healthy population. Associazione Medica Sabin.

Several studies have shown that insulin resistance and hyperinsulinemia are associated with many metabolic disorders predisposing to coronary heart disease (CHD). This syndrome has been termed syndrome X. However, it is not completely known whether these relationships are still present in the elderly, or whether other factors such as age, gender, and body fat distribution modulate them. Therefore, we investigated the relationship between fasting plasma insulin, total and regional adiposity, fasting plasma glucose and lipids, plasma plasminogen activator inhibitor-1 (PAI-1), fibrinogen, and coagulation factor VII in a sample of 100 healthy free-living octogenarians-nonagenarians (52 men and 48 women) who were disability-free according to the Katz index. By univariate analysis, fasting insulin correlated positively with all anthropometric measures except the waist to hip ratio (WHR) in women. There was a positive correlation between fasting insulin and fasting glucose (r=.40, P < .01), plasma triglycerides ([TGs] r=.21, P < .05), and PAI-1 levels (r=.33, P < .01), whereas a negative relation was found with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein, A-I (apo A-I) levels (r=-.22 and =-.24, respectively, P < .05). These relationships were weaker and less significant in women. In pooled data, stepwise multiple regression analysis showed an independent relationship of both the body mass index (BMI) and fasting insulin level with TGs (R2=.14), while gender and fasting insulin were the best predictors of HDL-C variance (R2=.17). Furthermore, fasting insulin was the only variable independently related to PAI-1 (R2=.12). Our findings support the existence of a metabolic syndrome even in very old age by showing that high insulin levels are related to various metabolic and hemostatic disorders.

Age Factors↗

Fasting-induced apoptosis in rat liver is blocked by cycloheximide.

The effect of cycloheximide (CH) on the fasting-induced changes of rat liver cell and protein turnover has been investigated. Late starvation phase (3-4-day-fasting period) was characterised by a decrease in liver weight and protein and DNA content. The loss of DNA was not related to liver cell necrosis but due not only to depression of cell proliferation as shown by the drop in the labelling index but also induction of apoptosis. This type of apoptosis was documented by the increase in the apoptotic index (cells labelled by TUNEL) and transglutaminase activity as well as by DNA fragmentation. The liver cells of fasted rats appeared smaller as shown by the higher cell density and DNA/protein ratio than in controls. Females were more resistant to fasting-induced apoptosis than males. A single dose of CH, a drug primary known as inhibitor of protein synthesis, induced or enhanced apoptosis in fed and 2-days fasted male rats, respectively, without any sign of cell necrosis. On the contrary, the administration of repeated doses of CH blocked apoptosis induced by fasting. CH "froze" protein and DNA content as well as apoptotic process at the level of 2 days-fasted rats. While fasting-induced liver protein loss resulted from a marked reduction in protein synthesis with a slight decrease in degradation, repeated treatment with CH virtually blocked protein loss by abolishing protein catabolism. These data suggest a direct relationship between the catabolic side of protein turnover and the apoptotic process.

Animals↗

The decrease of liver LDL receptor mRNA during fasting is related to the decrease in serum T3.

UNLABELLED: Fasting is associated with a reduction in serum T3 and T4 and a rise of plasma LDL cholesterol. We hypothesized that an hypothyroid-like condition induced by fasting is responsible for the rise in LDL cholesterol. We therefore examined the relation between changes in thyroid hormone and cholesterol metabolism in rats fasted for 0, 8, 12, 24 or 48 h. Fasting resulted in a decrease of liver 5'-deiodinase mRNA from 8 h (to 50%, p < 0.05, n = 6), of serum T3 from 12 h and of serum T4 at 48 h; serum TSH remained unchanged. Furthermore, plasma LDL cholesterol increased from 24 h onwards preceded by a decrease of liver LDL receptor mRNA which in turn is related to serum T3 (r = 0.55, p < 0.05, n = 19). Adding T3 at a concentration such that normal T3 levels are maintained during 48 h fasting, prevents the decrease in the LDL receptor mRNA. Fasting did not change hepatic HMG CoA reductase mRNA but decreased cholesterol 7 alpha-hydroxylase mRNA, which however was not related to the decrease of serum T3. IN CONCLUSION: (1) Fasting induces a hypothyroid-like condition in which inhibition of hepatic conversion of T4 into T3 may be responsible for the decrease of serum T3. (2) Fasting induces an increase of plasma LDL cholesterol, apparently caused by a decrease of hepatic LDL receptor gene expression which is (partly) related to the fall in serum T3.

Animals↗

Developmental changes in the activation properties and ultrastructure of fast- and slow-twitch muscles from fetal sheep.

At early stages of muscle development, skeletal muscles contract and relax slowly, regardless of whether they are destined to become fast- or slow-twitch. In this study, we have characterised the activation profiles of developing fast- and slow-twitch muscles from a precocial species, the sheep, to determine if the activation profiles of the muscles are characteristically slow when both the fast- and slow-twitch muscles have slow isometric contraction profiles. Single skinned muscle fibres from the fast-twitch flexor digitorum longus (FDL) and slow-twitch soleus muscles from fetal (gestational ages 70, 90, 120 and 140 days; term 147 days) and neonatal (8 weeks old) sheep were used to determine the isometric force-pCa (pCa = -log10[Ca2+]) and force-pSr relations during development. Fast-twitch mammalian muscles generally have a greatly different sensitivity to Ca2+ and Sr2+ whereas slow-twitch muscles have a similar sensitivity to these divalent cations. At all ages studied, the force-pCa and force-pSr relations of the FDL muscle were widely separated. The mean separation of the mid-point of the curves (pCa50-pSr50) was approximately 1.1. This is typical of adult fast-twitch muscle. The force-pCa and force-pSr curves for soleus muscle were also widely separated at 70 and 90 days gestation (pCa50-pSr50 approximately 0.75); between 90 days and 140 days this separation decreased significantly to approximately 0.2. This leads to a paradoxical situation whereby at early stages of muscle development the fast muscles have contraction dynamics of slow muscles but the slow muscles have activation profiles more characteristic of fast muscles. The time course for development of the FDL and soleus is different, based on sarcomere structure with the soleus muscle developing clearly defined sarcomere structure earlier in gestation than the FDL. At 70 days gestation the FDL muscle had no clearly defined sarcomeres. Force (N cm-2) increased almost linearly between 70 and 140 days gestation in both muscle types and there was no difference between the Ca(2+)- and Sr(2+)-activated force throughout development.

Animals↗

Morphometric and biomechanical intestinal remodeling induced by fasting in rats.

The function of the small intestine is mechanical to a large degree. To understand the function it is necessary to know how the mechanical stresses and strains can be computed. Nutrition plays an important role in the maintenance of normal gut structure and function. The small intestine undergoes functional changes when food is withheld. To explore the morphological and biomechanical remodeling during starvation, intestinal segments from the fed and fasted rat duodenum, jejunum, and ileum were investigated. After seven days of fasting the animals lost 22% of the body weight and the intestinal mass per length decreased by nearly 40% in the duodenum. Fasting decreased the plasma levels of glucose, insulin, triglyceride, and cholesterol whereas the level of free fatty acids increased (P < 0.001). Fasting decreased the outer circumferential length, wall thickness, wall area, inner circumferential length, and luminal area at the three locations (P < 0.001). Histological examination showed that the mucosal and the submucosal thickness decreased during fasting (P < 0.001), whereas the muscle layers were unchanged. The residual strain on the mucosal surface was compressive. The serosal residual strain was tensile and increased with the highest values after four days of fasting in the duodenum and jejunum (P < 0.001). Fasting shifted the stress-strain curves to the right in both circumferential and longitudinal directions at the three locations (P < 0.04). In conclusion pronounced biomechanical and structural remodeling occurred in the small intestine during fasting for up to one week. Since the contractile properties depend on the passive properties (according to the well-known Hill's model), it can be predicted that the smooth muscle contractile function will also change.

Biomechanical Phenomena↗

Effect of fasting and obesity in humans on the 6-hydroxylation of chlorzoxazone: a putative probe of CYP2E1 activity.

BACKGROUND AND OBJECTIVES: The hepatic 6-hydroxylation of chlorzoxazone in vitro is mediated primarily by CYP2E1, and measurement of this metabolic pathway may provide an in vivo probe of the enzyme. In animals, such as the rat, levels of CYP2E1 are induced by both fasting and obesity. This study investigated whether these two physiologic factors are determinants of the metabolism and disposition of chlorzoxazone in humans. METHODS: The plasma concentration-time profiles of chlorzoxazone and its 6-hydroxy metabolite were determined after oral administration of parent drug (250 mg). The urinary excretion of the metabolite was also determined. In one study, the disposition profiles were obtained in six healthy white men, first after an overnight fast, and on a separate occasion after a 38-hour fast. The second study investigated the disposition of chlorzoxazone in nine obese women and in nine age-matched women. RESULTS: Prolonged fasting produced a significant increase in circulating ketone bodies. This was associated with a reduction in the oral clearance of chlorzoxazone (mean +/- SD, 5.79 +/- 1.04 to 3.69 +/- 1.54 ml.min-1.kg-1; p < 0.03). The 0- to 24-hour urinary recovery of the 6-hydroxy metabolite was extensive (50% to 80%), and the reduced clearance reflected a lower 6-hydroxylating ability after fasting. The elimination half-life of the drug was increased by a similar extent to clearance (1.00 +/- 0.09 versus 1.50 +/- 0.42 hours; p < 0.004), whereas its apparent volume of distribution was unaffected by fasting. By contrast, obesity resulted in significant increases in the oral clearance and distribution of chlorzoxazone on both an absolute and weight-normalized basis; for example, 4.15 +/- 0.81 versus 6.23 +/- 1.72 ml.min-1.kg-1 and 0.50 +/- 0.28 versus 0.82 +/- 0.19 L.kg-1. Half-life of elimination was similar in both groups of subjects. Estimation of the fractional clearance of 6-hydroxychlorzoxazone showed that obesity increased this parameter to a similar extent as oral clearance. The difference in the oral clearance and 6-hydroxylating ability of nonobese men and women was also statistically different. CONCLUSIONS: A discordancy was observed between the reported effect of fasting in rodents and that observed in humans. This may reflect an interspecies difference in CYP2E1 regulation or, more likely, destruction of the enzyme by lipid peroxidation resulting from the prolonged period of fasting. However, serious to morbid obesity in humans is associated with increased 6-hydroxylation of chlorzoxazone, consistent with induction of CYP2E1. Accordingly, such individuals may be at increased risk of CYP2E1-mediated toxicities and adverse effects caused by the formation of CYP2E1-mediated metabolites of environmental agents. In addition, the efficacy of an active drug that is a CYP2E1 substrate may be reduced in obese patients.

Adult↗

Differential effects of bepridil on functional properties of troponin C in slow and fast skeletal muscles.

1. Bepridil (BPD) is a pharmacological compound able to bind to the Ca2+ sensor protein troponin C (TnC), which triggers skeletal muscle contraction upon Ca2+-binding. BPD can thereby modulate the Ca2+-affinity of this protein. 2. The Ca2+-sensitizing action of bepridil was investigated on slow and fast isoforms of TnC from skinned slow and fast skeletal muscle fibres, activated by either Ca2+ or Sr2+ ions. 3. Bepridil did not modify the Ca2+ maximal tension of slow and fast fibres, suggesting that binding of the drug to TnC did not induce a change in the number of cross-bridges involved in maximal tension. 4. Sr2+ ions induced lower maximal tension than Ca2+ ions. However, in fast fibres, these lower Sr2+ maximal tensions could be reinforced by bepridil, suggesting an effect of bepridil on the function of site I of fast TnC. 5. Under submaximal tension, bepridil induced an increase in Ca2+ affinity of TnC in both slow and fast fibres. However, slow fibres were more drug reactive than fast fibres, and the increase in tension appeared to be modulated by the Ca2+ concentration. 6. Thus, bepridil exerted a differential effect on slow and fast fibres. Moreover, the results suggest that bepridil was more effective when activation conditions were unfavourable.

Animals↗

Appetite sensations and eating behaviors to complete fasting in obese and non-obese individuals.

OBJECTIVE: To investigate the response of appetite sensations and eating behaviors to fasting in obese and non-obese individuals. DESIGN: Prospective study on inpatients enrolled in weight loss program including fasting at the obesity clinic, an oriental medical center in Seoul, Korea. SUBJECTS AND MEASUREMENTS: For seven obese (body mass index BMI> or =30) and 11 non-obese (BMI<30) patients, the modified visual analog scale (VAS) was administered three times per day throughout 9 days of complete fasting. Three-Factor Eating Questionnaire (TEEQ) was administered before and 18 days after the complete fasting period. RESULTS: After treatment, average weight losses were 7.4 kg (3.0 BMI) for the obese group and 6.7 kg (2.6 BMI) for the non-obese. TFEQ scales did not differ by weight status at both before and after treatments. Eighteen days after the fasting, an increase of restraint of eating was found only for the non-obese. There was a decrease of disinhibition of eating regardless of weight status. During fasting, desire to eat, hunger and prospective consumption decreased for the non-obese, while these appetite sensations tended to increase slightly for the obese. CONCLUSIONS: BMI, independent of dieting status, appeared to be related to appetite sensations except for satiety during fasting, but not before and 18 days after fasting.

Adult↗

Leptin increases circulating glucose, insulin and glucagon via sympathetic neural activation in fasted mice.

OBJECTIVE: A number of recent studies suggest that leptin has effects on glucose metabolism and pancreatic hormone secretion. Therefore, the effect of leptin administration on circulating glucose, insulin and glucagon in fed and fasted mice was investigated. The potential contribution of the sympathetic nervous system to the effects of leptin was also examined. DESIGN: Recombinant human or murine leptin was administered intraperitoneally (300 microg/mouse per 12 h over 24 h) to fed or fasted, normal or chemically sympathectomized NMRI mice. Blood samples were collected at baseline and after 24 h. MEASUREMENTS: Plasma concentrations of glucose, insulin and glucagon. RESULTS: In the fed state (n = 24), leptin administration did not affect glucose, insulin or glucagon concentrations after 24 h. Fasting (n = 24) reduced body weight by 2.2+/-0.4 g, plasma glucose by 3.7+/-0.4 mmol/l, plasma insulin by 138+/-35 pmol/l, and plasma glucagon by 32+/-7 pg/ml. In fasted mice, human leptin (n = 24) increased plasma glucose by 1.5+/-0.2 mmol/l (P = 0.041), plasma insulin by 95+/-22 pmol/l (P = 0.018), and plasma glucagon by 16+/-3 pg/ml (P = 0.025), relative to saline-injected control animals. Murine leptin exerted similar stimulating effects on circulating glucose (+1.0+/-0.2 mmol/l, P = 0.046), insulin (+58+/-17 pmol/l, P = 0.038) and glucagon (+24+/-9 pg/ml, P = 0.018) as human leptin in fasted mice (n = 12) with no significant effect in fed mice (n = 12). Human leptin did not affect circulating glucose, insulin or glucagon in fasted mice after chemical sympathectomy with 6-hydroxydopamine (40 mg/kg iv 48 h prior to fasting; n = 12). CONCLUSION: Leptin increases circulating glucose, insulin and glucagon in 24 h fasted mice by a mechanism requiring intact sympathetic nerves.

Animals↗

Compared with nibbling, neither gorging nor a morning fast affect short-term energy balance in obese patients in a chamber calorimeter.

OBJECTIVE: To test if a diet of 4.2 MJ/24 h as six isocaloric meals would result in a lower subsequent energy intake, or greater energy output than (a) 4.2 MJ/24 h as two isocaloric meals or (b) a morning fast followed by free access to food. DESIGN: Subjects were confined to the Metabolic Unit from 19:00 h on day 1 to 09:30 h on day 6. Each day they had a fixed diet providing 4.2 MJ with three pairs of meal patterns which were offered in random sequence. They were: six meals vs two meals without access to additional foods (6vs2), or six meals vs 2 meals with access to additional food (6+vs2+), or six meals vs four meals (6+vsAMFAST). In the AMFAST condition the first two meals of the day were omitted to reduce daily intake to 2.8 MJ and to create a morning fast, but additional food was accessible thereafter. Patients were confined in the chamber calorimeter from 19:00 h on day 2 until 09:00 h on day 4, and then from 19:00 h on day 4 to 09:00 h on day 6. The order in which each meal pattern was offered was balanced over time. MEASUREMENTS: Energy expenditure (chamber calorimetry), spontaneous activity (video) and energy intake (where additional foods were available) during the final 24 h of each dietary component. SUBJECTS: Ten (6vs2), eight (6+vs2+) and eight (6+vsAMFAST) women were recruited who had a BMI of greater than 25 kg/m2. RESULTS: From experiment 6vs2 the difference between energy expenditure with six meals (10.00 MJ) and two meals (9.96 MJ) was not significant (P=0.88). Energy expenditure between 23:00 h and 08:00 h ('night') was, however, significantly higher (P=0.02) with two meals (9.12 MJ/24 h) compared with six meals (8.34 MJ/24 h). The pattern of spontaneous physical activity did not differ significantly between these two meal patterns (P>0.05). Total energy intake was affected by neither meal frequency in experiment 6+vs2+ (10.75 MJ with six, 11.08 MJ with two; P=0.58) nor a morning fast in experiment 6+vsAMFAST (8.55 MJ/24 h with six, 7.60 MJ with AMFAST; P=0.40). The total diet of subjects who had a morning fast tended to have a lower percentage of total energy from carbohydrate (40%) than when they had six meals per 24 h (49%) (P=0.05). Subsequent energy balance was affected by neither meal frequency (6vs2; P=0.88, 6+vs2+; P=0.50) nor a morning fast (P=0.18). CONCLUSIONS: In the short term, meal frequency and a period of fasting have no major impact on energy intake or expenditure but energy expenditure is delayed with a lower meal frequency compared with a higher meal frequency. This might be attributed to the thermogenic effect of food continuing into the night when a later, larger meal is given. A morning fast resulted in a diet which tended to have a lower percentage of energy from carbohydrate than with no fast.

Adult↗

Blunted fasting-induced decreases in plasma and CSF leptin concentrations in obese rats: the role of increased leptin secretion.

Fasting substantially decreases plasma leptin concentration. However, in obesity, the fasting-induced decrease in leptin concentration is blunted or absent. The objective of the current study was to determine in diet-induced obese (DIO) rats the contribution of altered leptin secretion and leptin expression to the blunted nutritional regulation of leptin concentration. Fasting-induced decreases in plasma leptin concentration were greater in lean (standard chow (SC)) rats compared to DIO (approximately 79 vs approximately 48%, P<0.05 for DIO vs SC). CSF leptin was significantly reduced by fasting in SC (approximately 46%) but not in DIO. Fasting decreased adipose tissue leptin secretion in both SC and DIO, but the decrease was greater in SC (average approximately 74%) compared to DIO (average approximately 44%, P<0.05, DIO vs SC). Additionally, leptin secretion in fasted DIO was substantially greater (average approximately 175%) than in fasted SC (P<0.05). Adipose tissue leptin protein content was increased by approximately 80% in DIO compared to SC (P<0.05). We conclude that a probable cause of blunted fasting-induced decreases in leptin concentration in obesity is elevated leptin secretion, which possibly results from increased leptin gene expression.

Adipose Tissue↗

Serum adiponectin concentrations during a 72-hour fast in over- and normal-weight humans.

OBJECTIVE: Adiponectin is currently considered an important link between obesity and insulin resistance, since circulating levels of this insulin sensitizing hormone have consistently been found to be reduced in obese subjects. However, until now it is not known how the secretion of adiponectin is regulated in response to acute metabolic changes. Here, we assessed the influence of complete fasting for 72 h on serum adiponectin levels. DESIGN: Between group comparison of repeated measurements. SUBJECTS: In total, 18 normal-weight (mean+/-s.e.m. BMI: 22.2+/-0.4 kg/m(2); age: 39.2+/-4.4 y) and nine over-weight (BMI: 33.2+/-1.8 kg/m(2); age: 36.9+/-4.5 y) subjects. MEASUREMENTS: Serum adiponectin levels were measured every 4 h during a 72-h fasting period. Additionally, concentrations of plasma glucose and serum insulin and leptin were assessed at the beginning and in the end of the fasting experiment. Insulin resistance was estimated using the homeostasis model assessment (HOMA). RESULTS: While concentrations of glucose, insulin, and leptin decreased across the fasting period by 31.0, 33.1 and 60.0%, respectively (all P<0.005), adiponectin levels remained unchanged (P=0.817). Overall, over-weight subjects exhibited slightly lower adiponectin levels than normal-weight subjects (P=0.092), but there was no difference in the time course of adiponectin levels during fasting between these two groups (P=0.970). Although, averaged adiponectin levels before and after fasting did not systematically differ, individual changes in adiponectin levels across fasting displayed a slight but significant inverse correlation with changes in plasma glucose concentration (r=-0.42, P=0.03). DISCUSSION: The data show that serum adiponectin concentrations remain remarkably stable during 72 h of fasting in normal- and over-weight subjects. Thus, adiponectin appears to reflect primarily long-term changes in body weight with little evidence for a dependence on short-term regulatory influences.

Adiponectin↗

The effect of fasting on the activation in vivo of the insulin receptor kinase.

Fasting causes insulin resistance in liver and fat, and increases insulin sensitivity in muscle. We studied the response in vitro and in vivo to insulin of the insulin receptor tyrosine kinase in muscle and liver from 72 h fasted and control rats. Insulin was injected intraperitoneally together with glucose, and blood and tissue samples were obtained 0, 5, 15 and 30 min later. Basal serum glucose and insulin levels were significantly higher in control than in fasting rats. Serum glucose rose to approximately 300 mg/dl at 5 min and then progressively declined without hypoglycaemia. Receptors were prepared from whole tissue by wheat germ lectin affinity chromatography. 125I-insulin binding to purified receptors was increased by fasting in both muscle (18%) and liver (50%). In untreated fasting and control animals, muscle and liver insulin receptor tyrosine kinase activity was stimulated to similar levels by insulin added in vitro. With only insulin treatment in vivo, muscle receptor tyrosine kinase behaved similarly in fasting and control animals with maximal activation at 15 min post injection. In liver, insulin in vivo stimulated receptor tyrosine kinase activity maximally at 5 min post injection in both fasting and control, but in fasting animals the treatment in vivo caused a significantly larger and more prolonged activation of the enzymic activity, possibly due to a decrease in the rate of dephosphorylation and deactivation of the beta subunits.

Animals↗