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PubMed2001

Glucose facilitation of cognitive performance in healthy young adults: examination of the influence of fast-duration, time of day and pre-consumption plasma glucose levels.

RATIONALE: Previous investigations have demonstrated increased performance after the administration of a glucose-load on certain aspects of cognitive functioning in healthy young adults. Generally these studies have used a procedure where participants were tested in the morning after an overnight fast. OBJECTIVE: The aim of the present study was, for the first time, to investigate the glucose cognitive facilitation effect under more natural testing times and with shorter duration of the previous fast. METHODS: Measures of verbal and non-verbal memory performance were compared under different fasting intervals (2-h fast versus overnight fast), times (morning versus afternoon) and glycaemic conditions (glucose versus aspartame drinks) in healthy young participants. RESULTS: There was a significant glucose facilitation effect on long-term verbal memory performance. In addition, glucose significantly enhanced long-term spatial memory performance. The effect of glucose was essentially equivalent whether it was given after an overnight fast or a 2-h fast following breakfast or lunch. There was no effect of drink and time of day on working memory performance. CONCLUSIONS: The results of this study further support the hypothesis that glucose administration can enhance certain aspects of memory performance in healthy young adults. More significantly, the findings indicate that this cognitive facilitation effect persists under more naturalistic conditions of glucose administration and is not restricted to long fast durations or morning administration.

Adolescent↗
PubMed1997

Hormonal and metabolic adaptations to fasting in monosodium glutamate-obese rats.

The effect of fasting on hormonal and metabolic variables was evaluated in normal rats and in rats with obesity induced by neonatal treatment with monosodium glutamate (MSG). The hyperinsulinemia of the fed obese rats was reversed by fasting. Plasma corticosterone was also high in the fed obese and decreased to levels similar to fed controls, while it increased in the latter group during fasting. In contrast, thyroid hormone levels decreased in controls but increased in the obese rats in response to fasting. The fed obese group had lower carcass protein and higher carcass lipid contents than controls. In response to fasting, the decrements of the initial amount of both protein and fat were lower in MSG than in controls. Fasting induced a sustained increase in plasma free fatty acids only in the obese rats, although a single 100 mumol.l-1 dose of norepinephrine stimulated in vitro glycerol release more pronouncedly in epididymal adipocytes from control than obese rats. The results indicate that MSG-obese rats were able to mobilize fat stores during prolonged fasting. The high availability of lipid fuels and the sharp and sustained decrease in circulating corticosterone in the MSG group were probably important in diminishing body protein consumption during fasting.

Adaptation, Physiological↗
PubMed2006

Time-dependent modulation of rat serum paraoxonase 1 activity by fasting.

High-density lipoprotein-associated paraoxonase 1 (PON1) protects the endothelium from the pro-oxidant activity of oxidised low-density lipoprotein. Whereas fasting has been related to increased oxidative stress, intermittent fasting and caloric restriction are associated to increased resistance to oxidative injury. Taking into consideration that serum PON1 activity is modulated by a restriction of caloric intake and because there is no evidence regarding PON1 response to total food deprivation, we investigated whether PON1 activity is involved in the response aimed to counteract the greater oxidative stress associated to fasting and whether serum PON1 activity is altered by the length of food deprivation. Male Wistar rats were randomly divided into five groups: fed and 6-, 12-, 24- or 48-h fasted rats. Serum PON1 activity increases within the first hours of fasting, representing a prompt adaptation designed to attenuate blood lipid peroxidation that cannot be sustained when fasting is prolonged. This PON1 response to early fasting could be part of the mechanisms triggered by periodically repeated short periods of food deprivation - intermittent fasting - which result in increased resistance to stress by stimulating antioxidant defences.

Animals↗
PubMed2002

Differential expression of two MyoD genes in fast and slow muscles of gilthead seabream ( Sparus aurata).

Members of the myogenic regulatory gene family, including MyoD, Myf5, Myogenin and MRF4, are specifically expressed in myoblast and skeletal muscle cells and play important roles in regulating skeletal muscle development and growth. They are capable of converting a variety of non-muscle cells into myoblasts and myotubes. To better understand their roles in the development of fish muscles, we have isolated the MyoD genomic genes from gilthead seabream (Sparus aurata), analyzed the genomic structures, patterns of expression and the regulation of muscle-specific expression. We have demonstrated that seabream contain two distinct non-allelic MyoDgenes, MyoD1 and MyoD2. Sequence analysis revealed that these two MyoD genes shared a similar gene structure. Expression studies demonstrated that they exhibited overlapping but distinct patterns of expression in seabream embryos and adult slow and fast muscles. MyoD1 was expressed in adaxial cells that give rise to slow muscles, and lateral somitic cells that give rise to fast muscles. Similarly, MyoD2 was initially expressed in both slow and fast muscle precursors. However, MyoD2 expression gradually disappeared in the adaxial cells of 10- to 15-somite-stage embryos, whereas its expression in fast muscle precursor cells was maintained. In adult skeletal muscles, MyoD1 was expressed in both slow and fast muscles, whereas MyoD2 was specifically expressed in fast muscles. Treating seabream embryos with forskolin, a protein kinase A activator, inhibited MyoD1 expression in adaxial cells, while expression in fast muscle precursors was not affected. Promoter analysis demonstrated that both MyoD1 and MyoD2 promoters could drive green fluorescence protein expression in muscle cells of zebrafish embryos. Together, these data suggest that the two non-allelic MyoD genes are functional in seabream and their expression is regulated differently in fast and slow muscles. Hedgehog signaling is required for induction of MyoDexpression in adaxial cells.

Amino Acid Sequence↗
PubMed2005

Current practice of preoperative fasting: a nationwide survey in Japanese anesthesia-teaching hospitals.

PURPOSE: We conducted a nationwide survey to investigate the current practice of the preoperative fasting period in Japanese anesthesia-teaching hospitals. Acceptance of the clinical practice guideline published by the American Society of Anesthesiologists (ASA) was also surveyed. METHODS: A written type of questionnaire was mailed to 795 teaching hospitals. RESULTS: The response rate of the questionnaires was 57%. Most (>90%) of the respondents had been applying a longer fasting period than the ASA-recommended minimum period specifically in adults; the median duration of fasting was 12-13 h for solids and 6-9 h for liquids. Children or infants were allowed a more liberalized fasting period, frequently being permitted an oral intake of clear fluids up to 3 h before anesthesia. The incidence of pulmonary aspiration was 1/12,500 general anesthesia cases, and application of the ASA guideline appeared not to affect the incidence. Japanese anesthesiologists were still reluctant to depart from their traditional long fasting periods, as most of them could find little benefit in reducing the fasting periods. CONCLUSION: The long preoperative fasting period is still common practice in Japanese anesthesia-teaching hospitals. A national guideline for a preoperative fasting policy is worth exploring to change the current practice.

Anesthesia↗
PubMed2005

TGF-beta1 favors the development of fast type identity during soleus muscle regeneration.

Transforming growth factor-beta1 (TGF-beta1) is known to be expressed in the environment of developing fast muscle fibres during ontogenesis. In the present study, we have examined effects of administration of either TGF-beta1 or neutralizing TGF-beta1 antibody on the induction of fast type phenotype in regenerating skeletal muscles in rats. Expressions of fast and slow myosin heavy chain (MHC) isoforms were studied using protein electrophoresis, at 3 and 6 weeks after myotoxic treatment. Muscle contractile properties were also measured in situ. The results have shown that a single injection of TGF-beta1 into the regenerating slow soleus muscle increased the expression of fast MHC-2x/d and MHC-2a and decreases that of slow MHC-1 (P<0.05). Moreover, it reduced the degree of tetanic fusion during contraction (P<0.05). Conversely, injection of neutralizing antibody against TGF-beta1 into the regenerating fast EDL muscle increased the expression of MHC-2a and MHC-1 (P<0.05). In conclusion, when the slow muscle was regenerating in the presence of an increased level of TGF-beta1, it induced a shift to a less slow MHC phenotype and contractile characteristics. Conversely, neutralization of TGF-beta1 in the regenerating fast muscle induced a shift to a less fast MHC expression. Together these results suggest that TGF-beta1 influences some aspects of fast muscle-type patterning during skeletal muscle regeneration.

Animals↗
PubMed1985

Endogenous plasma lipoprotein lipase activity in fed and fasting rats may reflect the functional pool of endothelial lipoprotein lipase.

In this study, a correlation was sought between the circulating lipoprotein lipase activity and nutritional state in the rat. In fed rats, the plasma lipoprotein lipase activity was between 30 and 120 munits/ml, whereas after an overnight fast in restraining cages, the lipoprotein lipase plasma levels were between 280 and 500 munits/ml. The plasma lipoprotein lipase activity was inhibited by a specific high titre goat antiserum to rat lipoprotein lipase. No effect of fasting was seen on the plasma hepatic triacylglycerol lipase. 6 h after fasting, adipose tissue lipoprotein lipase decreased maximally, but plasma lipoprotein lipase was not changed and rose only after 16 h. Thus, it seems that most of the lipoprotein lipase activity in the fasting plasma was related to the 3-fold rise in lipoprotein lipase activity in the heart, which may represent total muscle lipoprotein lipase. The increase in heart lipoprotein lipase was due in part to an increase in the t1/2 of the enzyme from 1.2 to 2.9 h. To determine whether the high plasma levels in the fasting rats might result from impaired clearance of the enzyme by the liver, functional hepatectomy was carried out. 15 min after hepatectomy, plasma lipoprotein lipase rose up to 20-fold in fed and about 6-fold in fasting rats. Lipoprotein lipase activity extracted by the liver was calculated to be 30-60 munits/ml in the fed and 171-247 munits/ml plasma per min in fasting rats. An increase in lipoprotein lipase activity in extrahepatic tissues (heart, lung, kidney, diaphragm and adrenal) occurred 30 min after hepatectomy in fed rats. The increase in heart lipoprotein lipase was due to an increase in heparin-releasable fraction. Since no impairment of hepatic clearance of circulating plasma lipoprotein lipase was found, the high fasting plasma lipoprotein lipase activity may be related to an increase in enzyme synthesis, decreased enzyme turnover and an expansion of the functional pool in tissues such as the heart and probably muscle. The present findings indicate that measurement of endogenous plasma lipoprotein lipase can provide information with respect to the size of the functional pool under normal and pathological conditions.

Animals↗
PubMed1986

Anomalous susceptibility of the fasted hamster to acetaminophen hepatotoxicity.

The effect of an acute fast on susceptibility to acetaminophen-induced hepatotoxicity was investigated in male Golden Syrian hamsters. Overnight starvation markedly elevated hepatic levels of glutathione throughout the diurnal cycle (peak concentration: 10.6 +/- 0.06 mM vs 7.3 +/- 0.3mM in controls). However, despite this apparent increase in the glutathione protective capacity of the liver, acetaminophen-induced hepatic necrosis was modestly potentiated by fasting, as judged by liver histology and elevation of serum transaminase (SGOT) activity. Parallel pharmacokinetic studies indicated that the overall elimination rate constant for acetaminophen was decreased in fasted animals, due largely to decreases in the apparent rate constants for formation of acetaminophen glucuronide and acetaminophen mercapturate. Formation of acetaminophen sulfate was not affected by fasting. Since the major nontoxic pathway (glucuronide) and the toxic pathway (as measured by mercapturate) decreased to a similar extent, the data indicate that the anomalous lack of protection cannot be explained on the basis of altered metabolic disposition of the drug. Measurement of hepatic glutathione levels revealed that, despite the higher initial level of glutathione in the fasted animals, the nadir to which liver glutathione levels fell after acetaminophen was the same in fed and fasted animals. Comparison of the amount of acetaminophen mercapturate in the urine with the amount of glutathione which disappeared from the liver showed close agreement for fed animals, but a major discrepancy for fasted hamsters. These data indicate that a major fraction of glutathione in the liver of the fasted hamsters is not utilized for detoxification of the acetaminophen reactive metabolite and hence does not contribute to the glutathione protective capacity.

Acetaminophen↗
PubMed1987

Mechanisms of fasting-induced potentiation of acetaminophen hepatotoxicity in the rat.

The effects of an acute fast on acetaminophen metabolism and hepatotoxicity were investigated in male Long Evans Hooded rats. Histologic studies confirmed that fasting potentiated acetaminophen-induced hepatic necrosis. The previous known fasting-induced decrease in hepatic levels of glutathione and depletion of glycogen levels were also confirmed. Pharmacokinetic studies revealed that, at high dose levels of acetaminophen, fasting decreased the overall rate of elimination as evidence by a longer blood half-life of the drug. The decreased clearance was largely the result of decreases in the apparent rate constants for glucuronidation (ca. 40%) and for sulfation (ca. 30%). Fasting had no significant effects on the apparent rate constants for formation of either acetaminophen mercapturate or the methylthio derivatives. The depression of the nontoxic glucuronidation and sulfation pathways resulted in an increased proportion of the dose converted to the toxic metabolite and, hence, contributed to the potentiation of liver injury in fasted rats. In addition, these studies demonstrated that significant glucuronidation capacity (ca. 60% of that in fed rats) was maintained in fasted rats, indicating that: the glucuronidation capacity was not directly correlated with glycogen levels; and in fasted rats the glucose required for UDP-glucuronic acid formation for acetaminophen glucuronidation was supplied from sources other than glycogen.

Acetaminophen↗
PubMed1993

Effects of ether anaesthesia and fasting on various cytochromes P450 of rat liver and kidney.

Fed and fasted, male, Wistar albino rats exposed to light ether anaesthesia and killed immediately or after 30 or 120 min recovery were compared with non-anaesthetized rats for changes in liver and kidney cytochrome P450 (CYP) activities. In fed rats, liver total CYP (nmol/mg protein) decreased by 30% immediately after ether, but was restored to normal levels after 30 min recovery; in fasted rats, liver total CYP increased by 20% by fasting alone, then decreased by 65% immediately after ether, and recovered to only 70% of control at 2 hr after ether. Rat liver cytochrome P4501A (CYP1A; 7-ethoxyresorufin O-deethylase or EROD activity) and cytochrome P4502B (CYP2B; 7-pentoxyresorufin O-dealkylase or PROD activity) were decreased after ether anaesthesia, similar to those for total CYP. In contrast, rat liver cytochrome P4502E1 (CYP2E1), determined by p-nitrophenol hydroxylation, increased by 40% by ether anaesthesia alone, 70% by fasting alone and 140% by ether plus fasting; these increases were confirmed by the CYP2E1-mediated activation of nitrosopyrrolidine and by immunoblot analysis using antibody to CYP2E1. In rat kidney, losses of total CYP, CYP1A and CYP2B, and increases of CYP2E1, induced by ether anaesthesia, were much more marked in fasted (90% loss in total CYP, 30% increase in CYP2E1) than in fed rats (slight loss in total cytochrome P450, 30% increase in CYP2E1). As maximum losses of total CYP in liver of fasted rats exposed to ether occurred at the time of maximum increase of CYP2E1 and maximum rate of generation of reactive oxygen species (ROS), it is suggested that the increase of CYP2E1, resulting from its stabilization by fasting and ether, leads to generation of ROS, increase in lipid peroxidation and consequent loss of total CYP, associated with the hepatic and renal necrosis seen in ether intoxication and surgical trauma.

Anesthesia, General↗
PubMed1996

Ventromedial hypothalamic lesions produced by gold thioglucose do not impair induction of NPY mRNA in the arcuate nucleus by fasting.

There is increasing evidence that neuropeptide Y (NPY) plays an important role in the regulation of food intake. Neuropeptide Y mRNA in the arcuate nucleus increases after fasting and it has been proposed that this increase in NPY activity occurs as a result of the decreased circulating levels of both insulin and glucose associated with a fast. Glucose-responsive neurons in the ventromedial nucleus (VMN) of the hypothalamus alter their activity in response to changes in circulating glucose levels and these neurons have been proposed to be involved in the regulation of feeding behavior and metabolism. However, it is not known if these glucose-responsive neurons are involved in the response of NPY mRNA in the arcuate nucleus to fasting. To address this relationship, mice were injected with either saline or gold thioglucose (GTG), which appears to act on glucose-responsive neurons, and killed 6 weeks later after a 72 h fast or under ad lib fed conditions. In situ hybridization histochemistry for NPY mRNA was performed on hypothalamic sections containing the arcuate nucleus. The number of labelled cells was counted and the density of autoradiographic silver grains overlying the cells was also quantified (i.e. pixels per cell). Fasting resulted in increased levels of total NPY mRNA (number of labelled cells multiplied by the pixels per cell) in the arcuate nucleus of both control and GTG-treated mice. In addition, the relative fasting-induced increase (i.e. the fasted to fed ratio) in number of cells detected, number of pixels per cell, and total NPY mRNA was similar in both the control and GTG-treated mice. These data suggest that GTG-sensitive VMN neurons play little role in the induction of NPY mRNA by fasting in the arcuate nucleus.

Animals↗
PubMed1975

Effect of thyroid hormone on metabolic adaptation to fasting.

The acute effect of triiodothyronine (T3) on mobilization of fat and protein energy stores has been measured in five fasting, normal men. Fasting subjects were chosen for this study to amplify catabolic effects occurring during brief thyroid hormone treatment. Subjects were fasted for 72 hr on two occasions with admintration of T3, 150 mug every 12 hr, for 72 hr before and during the second fast. Plasma beta hydroxybutyrate, acetoacetate, and free fatty acid levels as well as ketone, creatine, and urea excretion were measured during control and T3 fasts. T3 enhances catabolism of protein stores as indicated by the doubling of urea excretion during the T3 fasts. Likewise, creatine excretion is increased six to ninefold during the T3 fasts. Catabolism of fat stores is enhanced during the T3 fasts as shown by increased plasma free fatty acid and ketone levels, and increased ketone excretion. Brief T3 treatment for 3 days augments the expected protein and fat catabolism of starvation without causing subjective changes of hyperthyroidism. Much of the catabolic expression of hyperthyroidism may simply reflect inadequate caloric intake to fuel energy requiring processes stimulated by thyroid hormone such as cell membrane sodium pumping and protein synthesis.

Adult↗
PubMed1980

Nature of suppressed TSH secretion during undernutrition: effect of fasting and refeeding on TSH responses to prolonged TRH infusions.

TSH responses to 4-hr continuous TRH infusions of approximately 0.8 microgram/min were assessed during feeding (1500 Kcal), fasting, and refeeding (1500 Kcal) intervals in 9 euthyroid obese subjects. The total area under the TSH response curve was 1854 +/- 322 muU/ml . 4-hr during feeding, decreased to 1359 +/- 199 muU/ml . 4-hr (p less than 0.01) on the 10th day of fasting, and remained low, being 1405 +/- 185 muU/ml . 4-hr, despite refeeding a 1500 Kcal diet (40% carbohydrate, 40% fat, 20% protein) for 5 days. Baseline serum T3 concentrations were 167 +/- 11 ng/dl during feeding, 86 +/- 8 ng/dl during fasting, and 119 +/- 12 ng/dl during refeeding. The observed decreases in TSH release appeared to correlate with decreased biologic action on the thyroid gland since the net rise in T3 during the infusion was less in fasting and refeeding than in the control (fed) period. Basal serum rT3 levels were 42 +/- 5 ng/dl during feeding, rose as expected to 56 +/- 5 ng/dl during fasting (p less than 0.005), and were completely restored to normal during refeeding (36 +/- 5 ng/dl). These data suggest that: (1) TSH responsiveness to prolonged TRH infusion is diminished during fasting and does not return to control (fed) values despite 5 days of refeeding a 1500 Kcal diet; (2) net T3 increases observed during the TRH infusion are greater in the fed period than in the fasting or refeeding periods; and (3) 5 days of refeeding a 1500 Kcal diet (40% carbohydrate, 40% fat, 20% protein) did not return the T3 to its original fed value whereas rT3 was completely restored to control values. Lastly, since the TSH response was lower both during the early and late phases of the infusion, the decrease in delta TSH to a bolus of TRH during fasting appears to represent one manifestation of a more general suppression of TSH neogenesis associated with caloric deprivation.

Adult↗
PubMed1981

Preservation of glucose tolerance and insulin secretory response to repeated glucose levels by the feeding of minimal glucose during prolonged fasting.

The facilitation of glucose disposal (Staub-Traugott effect) and potentiation of serum insulin (IRI) concentration normally occurring after closely spaced intravenous glucose loads, are known to disappear after prolonged starvation. To study the effects of minimal amounts of glucose during fasting upon the insulin response and disposal of repeated intravenous glucose tolerance tests, obese volunteers were fasted for a mean of 25 +/- 2 days, while receiving either 8 or 16 gm of oral glucose every 6 hr, and compared to totally fasted subjects without glucose supplementation. Weight loss rate and the fall in basal IRI and glucose levels were similar to those of totally fasted subjects. However, the Staub-Traugott effect and insulin secretory dynamics after stimulation by repetitive intravenous glucose loading were preserved by this glucose modified fast, while baseline serum glucagon levels (IRG) were significantly lower, and the basal IRI/IRG ratios were thus unchanged from the fed state. IRG and free fatty acid suppression were similar in the fed and glucose modified fasted states. Lactic acid levels increased as expected after the repeated glucose injections in the fed state, but failed to do so after the prolonged modified fast until the second and third repetitive glucose loads, in which a significant rise coincided with accelerated glucose disposal. It is suggested that minimal amounts of carbohydrate during fasting preserve the insulin potentiating action of glucose, preferentially sparing a delayed releasable pool of insulin, while protecting the glucose utilization mechanisms, including increased glycolysis, responsible for the Staub-Traugott effect.

Adult↗
PubMed1989

Accelerated decline in hepatic glucose production during fasting in normal women compared with men.

Plasma glucose values have been reported to be lower in women than in men after a 72-hour fast. However, a comparison of glucose kinetics in fasting men and women has not been described. Therefore, five normal men and five normal women underwent sequential 3-3H-glucose infusions after both a 14- and a 64-hour fast. Plasma glucose levels fell similarly during the fast in men (5.23 +/- 0.03 v 3.96 +/- 0.14 mmol/L, P less than .01) and women (4.84 +/- 0.14 v 3.65 +/- 0.25 mmol/L, P less than .01). The fall in plasma glucose was associated with a significantly greater fall in glucose appearance (Ra) in women compared with men (P less than .05). Ra fell 15.8% +/- 3.0% in men (2.11 +/- 0.24 to 1.79 +/- 0.24 mg.kg-1.min-1, P less than .01) and 24.6% +/- 1.4% in women (2.22 +/- 0.17 to 1.67 +/- 0.12 mg.kg-1.min-1, P less than .001). During the fast, plasma glycerol, free fatty acids (FFA), and beta-hydroxybutyrate levels rose significantly and plasma alanine fell significantly in both sexes. Plasma glycerol levels were significantly higher in women compared with men after fasting (0.16 +/- 0.01 v 0.11 +/- 0.02 mmol/L, P less than .05). In addition, the transition from ambulation to bed rest demonstrated unexpected sex-related differences in glucose homeostasis after the 64-hour fast. During the two-hour equilibration period required for glucose kinetic studies (subjects reclining), significant decrements in glucose, FFA, and lactate were observed in the 64-hour fasted women but not in the men.(ABSTRACT TRUNCATED AT 250 WORDS)

Bed Rest↗
PubMed1990

Prolonged fasting as conditioned by prior protein depletion: effect on urinary nitrogen excretion and whole-body protein turnover.

To study the influence of previous dietary protein depletion on nitrogen (N) loss and protein turnover during a total fast, we measured plasma leucine kinetics and urinary N and 3-methylhistidine (3MH) excretion in obese and normal subjects. In one study, 10 moderately obese women fasted for 2 weeks after adaptation either to a normal maintenance intake of 80 g protein and 150% of estimated resting energy expenditure (control group), or to 10 days of a 950-kcal, 200-g carbohydrate, 4-g protein diet (depletion group), with measurement of postabsorptive (or fasting) plasma leucine turnover on the maintenance diet and after 3 and 10 days of fasting. As measured after 10 days of fasting, body N loss was blunted by 17% when preceded by the protein-deficient diet. Plasma leucine flux and oxidation of the control group increased in early fasting and decreased by 10 days, in accordance with previous reports. Results for the depletion group were similar in absolute magnitude, despite the preceding protein-deficient diet. In a second study of five normal men, leucine kinetics were measured on a maintenance diet, after 10 days of a protein-free diet, and after 3 days of fasting. After protein depletion, leucine flux decreased by 19% (P less than .05). After 3 days fasting, leucine flux was 16% higher than on the maintenance diet (P less than .05), but 44% higher than the value on the protein-free diet 3 days earlier (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Fasting↗
PubMed1992

Effect of short-term fasting on nocturnal melatonin secretion in obesity.

To investigate whether the function of pinealocytes is altered in obesity, nocturnal melatonin (MT) secretion was determined in nine healthy subjects and compared with that of eight obese individuals. Serum MT levels were measured every second hour between 6:00 PM and 8:00 AM, and total nocturnal MT secretion (as reflected by the MT incremental area), MT peak time, and nocturnal urinary MT excretion were determined. None of these parameters differed significantly in the two groups. The obese subjects were reinvestigated after 2 days of complete fasting. This caused a decrease in body weight and basal blood glucose levels of 2.6 +/- 0.2 kg (mean +/- SEM, P less than .001) and 1.5 +/- 0.2 mmol/L (P less than .001), respectively, whereas serum cortisol levels remained unchanged. Short-term fasting reduced nocturnal MT secretion, as evidenced by MT incremental areas, which were reduced from 2.01 +/- 0.26 before fasting to 1.64 +/- 0.26 nmol/L.h after fasting (P less than .02). MT secretion peaks were reached simultaneously, and urinary MT excretion values did not change significantly in fasting. To see whether glucose supplementation during short-term fasting would normalize nocturnal MT secretion, we gave an additional seven obese subjects eight small oral doses of glucose (each dose, 0.5 g/kg body weight) at regular intervals during a 2-day fast. Their body weight decreased by 2.8 +/- 0.4 kg (P less than .001), but blood glucose and cortisol concentrations were similar before and after the glucose-supplemented fast, as was the nocturnal MT secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Locomotor activity and utilization of energy reserves during fasting after ventromedial hypothalamic lesions.

The ventromedial hypothalamus (VMH) is known to be involved in the regulation of energy metabolism but it may also modulate locomotor activity. Since prolonged fasting is marked by a succession of changes in energy utilization and locomotor activity, it was hypothesized that VMH may be a critical link controlling mobilization of energy stores and/or behavioral changes in response to fasting. To test this, the changes in rate of body mass loss, body content in lipid and protein, and wheel-running activity were studied in fasted nonobese rats with VMH electrolytic lesions. Secondary effects of VMH obesity were ruled out by postoperative restricted feeding. During fasting, VMH lesions impaired neither the overall lipid mobilization nor the late rise in daily body mass loss, concomitant with the increase in net proteolysis. Despite that the onset of this late stage of fasting was significantly delayed in VMH vs. sham-operated rats (13 +/- 1 vs. 8 +/- 1 days, respectively), the final amount of reserve lipids (3 g) was closely similar in both groups: this is the first experimental evidence of the hypothesis of a lipidic set-point. These results indicate that VMH is not a critical link controlling the time-course of utilization of energy reserves. The increase in diurnal (and total) daily wheel-running observed in fasted sham-operated rats still occurred in fasted VMH rats but was significantly reduced and delayed. VMH nuclei and/or associated fibers are therefore involved in the fasting-induced rise in diurnal activity.

Animals↗