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PubMed2000

Cigarette smoking and risk for impaired fasting glucose and type 2 diabetes in middle-aged Japanese men.

BACKGROUND: The contribution of cigarette smoking to development of impaired fasting glucose and type 2 diabetes remains unclear. OBJECTIVE: To investigate the association of cigarette smoking with development of impaired fasting glucose and type 2 diabetes. DESIGN: Prospective cohort study. SETTING: Work site in Osaka, Japan. PARTICIPANTS: 1,266 Japanese male office workers 35 to 59 years of age who did not have impaired fasting glucose or type 2 diabetes and were not taking medication for hypertension at study entry. MEASUREMENTS: Fasting plasma glucose levels were measured at annual health examinations from May 1994 through May 1999. Impaired fasting glucose was defined as a fasting glucose level of at least 6.1 mmol/L (110 mg/dL) but less than 7.0 mmol/L (126 mg/dL). Type 2 diabetes was defined as a fasting glucose level of 7.0 mmol/L or more or current receipt of hypoglycemic medication. RESULTS: 87 and 54 men developed impaired fasting glucose and type 2 diabetes during 5,817 and 5,937 person-years follow-up, respectively. After controlling for potential predictors of diabetes, the relative risk for impaired fasting glucose compared with never-smokers was 1.62 (95% CI, 0.85 to 3.10) for ever-smokers, 1.14 (CI, 0.58 to 2.25) for persons who smoked 1 to 20 cigarettes/d, 1.33 (CI, 0.63 to 2.80) for those who smoked 21 to 30 cigarettes/d, and 2.56 (CI, 1.32 to 4.95) for those who smoked 31 or more cigarettes/d (P for trend for current smokers only = 0.013). The respective multivariate-adjusted relative risks for type 2 diabetes compared with never-smokers were 1.08 (CI, 0.34 to 3.42), 1.88 (CI, 0.71 to 5.00), 3.02 (CI, 1.15 to 7.94), and 4.09 (CI, 1.62 to 1,029) (P for trend for current smokers only < 0.001). The number of pack-years of exposure was also positively related to development of impaired fasting glucose and type 2 diabetes (P for trend = 0.039 and 0.002, respectively). The relative risk for impaired fasting glucose and type 2 diabetes in current smokers versus never-smokers was stronger among men with a body mass index less than 242 kg/m2 than among men with a body mass index of 24.2 kg/m2 or more, although the absolute risk was greater in more obese men. CONCLUSION: The number of cigarettes smoked daily and the number of pack-years of exposure seem to be associated with development of impaired fasting glucose and type 2 diabetes in middle-aged Japanese men.

Adult↗
PubMed2002

Effects of fasting on corticosterone production by zona fasciculata-reticularis cells in ovariectomized rats.

BACKGROUND: To investigate the function and mechanism of fasting on the production of corticosterone in vitro by zona fasciculata-reticularis (ZFR) cells from ovariectomized (OVX) rats. METHODS: Female rats were OVX for 4 days before decapitation. Rats were fed or fasted for 1 day before experiment. ZFR cells from fed and fasted rats were incubated with adrenocorticotropic hormone (ACTH), forskolin, 8-bromo-3',5'-cyclic adenosine monophosphate, SQ22536, nifedipine, chelerythrine chloride, trilostane or steroidogenic precursors at 37 degrees C for either 60 or 30 minutes. Corticosterone, pregnenolone concentrations in spent media, and the intracellular adenosine 3',5'-cyclic monophosphate (cAMP) concentration were determined by radioimmunoassay. The effects of fasting in response to ACTH on the protein expressions of steroidogenic acute regulatory protein (StAR) or cytochrome P450 side-chain cleavage enzyme (P450scc) in ZFR cells were determined by Western blot analysis. RESULTS: The concentration of plasma corticosterone in fasted rats was significantly higher than that in fed rats (P<0.01). One-day fasting significantly increased the responsiveness of ZFR cells to ACTH, forskolin, and precursor-stimulated corticosterone productions and to forskolin-stimulated cAMP accumulation. The corticosterone production was reduced in fasted group when adenylyl cyclase was inhibited by SQ22536. The fasting-enhanced level of corticosterone production in ZFR cells was decreased by the administration of nifedipine but not altered by that of chelerythrine chloride. Fasting significantly increased trilostane-stimulated production of pregnenolone in ZFR cells. The activities of enzymes which converting cholesterol, pregnenolone, progesterone, and deoxycorticosterone to corticosterone and the expressions of StAR in ZFR cells were greater in fasted rats than in fed rats. CONCLUSIONS: This study demonstrated that fasting increased the release of corticosterone and the accumulation of cAMP by rat ZFR cells. The action mediated through enhancing the responsiveness to ACTH stimulation, cAMP cascades and the activity of L-type calcium channels. The activities of steroidogenic enzymes including P450scc, 3beta-hydroxysteroid dehydrogenase, 21-hydroxylase, and 11beta-hydroxylase were all enhanced by the fasting treatment.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1992

Fast Na+ channels and slow Ca2+ current in smooth muscle from pregnant rat uterus.

Smooth muscle cells normally do not possess fast Na+ channels, but inward current is carried through two types of Ca2+ channels: slow (L-type) Ca2+ channels and fast (T-type) Ca2+ channels. Using whole-cell voltage clamp of single smooth muscle cells isolated from the longitudinal layer of 18-day pregnant rat uterus, depolarizing pulses, applied from a holding potential of -90 mV, evoked two types of inward current, fast and slow [8]. The fast inward current decayed within 30 ms, depended on [Na]o, and was inhibited by TTX (K0.5 = 27 nM). The slow inward current decayed slowly, was dependent on [Ca]o, and was inhibited by nifedipine. These results suggest that the fast inward current is a fast Na+ channel current, and that the slow inward current is a Ca2+ slow channel current. A fast-inactivating Ca2+ channel current was not evident. Thus, the ion channels which generate inward currents in pregnant rat uterine cells are TTX-sensitive fast Na+ channels and dihydropyridine-sensitive slow Ca2+ channels. The number of fast Na+ channels increased during gestation. The averaged current density increased from 0 on day 5, to 0.19 on day 9, to 0.56 on day 14, to 0.90 on day 18, and to 0.86 pA/pF on day 21. This almost linear increase occurs because of an increase in the fraction of cells which possess fast Na+ channels, and it is suggested that the fast Na+ current may be involved in spread of excitation. The Ca2+ channel current density also was higher during the latter half of gestation. These results indicate that the fast Na+ channels and Ca2+ slow channels in myometrium become more numerous as term approaches, and may facilitate parturition. Isoproterenol (beta-agonist) did not affect either ICa(s) or INa(f), whereas Mg2+ (K0.5 of 12 mM) and nifedipine (K0.5 of 3.3 nM) depressed ICa(s). Oxytocin had no effect on INa(f) and actually depressed ICa(s) to a small extent. Therefore, the tocolytic action of beta-agonists cannot be explained by an inhibition of ICa(s), whereas that of Mg2+ can be so explained. The stimulating action of oxytocin on uterine contractions is not due to stimulation of ICa(s). Figure 11 summarizes the possible mechanisms by which uterine contractility can be modulated. In contrast to vascular smooth muscle, neither ISO nor adenosine, which produce elevation of cyclic AMP, affected ICa and INa. Therefore, no arrow can be drawn between cA-PK/cG-PK and the Ca2+ slow channel.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed1992

Fast Na+ channels and slow Ca2+ current in smooth muscle from pregnant rat uterus.

Smooth muscle cells normally do not possess fast Na+ channels, but inward current is carried through two types of Ca2+ channels: slow (L-type) Ca2+ channels and fast (T-type) Ca2+ channels. Whole-cell voltage clamp was done on single smooth muscle cells isolated from the longitudinal layer of 18-day pregnant rat uterus. Depolarizing pulses, applied from a holding potential of -90 mV, evoked two types of inward current, fast and slow. The fast inward current decayed within 30 ms, depended on [Na]o, and was inhibited by TTX (K0.5 = 27 nM). The slow inward current decayed slowly, was dependent on [Ca]o (or Ba2+), and was inhibited by nifedipine. These results suggest that the fast inward current is a fast Na+ channel current, and that the slow inward current is a Ca2+ slow channel current. A fast-inactivating Ca2+ channel current was not evident. We conclude that the ion channels which generate inward currents in pregnant rat uterine cells are TTX-sensitive fast Na+ channels and dihydropyridine-sensitive slow Ca2+ channels. The number of fast Na+ channels increased during gestation. The averaged current density increased from 0 on day 5, to 0.19 on day 9, 0.56 on day 14, 0.90 on day 18, and 0.86 pA/pF on day 21. This almost linear increase occurs because of an increase in the fraction of cells which possess fast Na+ channels. The Ca2+ channel current density also was higher during the latter half of gestation. These results indicate that the fast Na+ channels and Ca2+ slow channels in myometrium become more numerous as term approaches, and we suggest that the fast Na+ current may be involved in spread of excitation. Isoproterenol (beta-agonist) did not affect either ICa(s) or INa(f), whereas Mg2+ (K0.5 of 12 mM) and nifedipine (K0.5 of 3.3 nM) depressed ICa(s). Oxytocin had no effect on INa(f) and actually depressed ICa(s) (but not IBa) to a small extent. Therefore, the tocolytic action of beta-agonists cannot be explained by an inhibition of ICa(s), whereas that of Mg2+ can be so explained. The stimulating action of oxytocin on uterine contractions cannot be explained by a stimulation of ICa(s).

Animals↗
PubMed2000

Exercise attenuates the fasting-induced transcriptional activation of metabolic genes in skeletal muscle.

Fasting elicits a progressive increase in lipid metabolism within skeletal muscle. To determine the effects of fasting on the transcriptional regulation of genes important for metabolic control in skeletal muscle composed of different fiber types, nuclei from control and fasted (24 and 72 h) rats were subjected to nuclear run-on analysis using an RT-PCR-based technique. Fasting increased (P < 0.05) transcription rate of the muscle-specific uncoupling protein-3 gene (UCP3) 14.3- to 21.1-fold in white gastrocnemius (WG; fast-twitch glycolytic) and 5.5- to 7.5-fold in red gastrocnemius (RG; fast-twitch oxidative) and plantaris (PL; mixed) muscles. No change occurred in soleus (slow-twitch oxidative) muscle. Fasting also increased transcription rate of the lipoprotein lipase (LPL), muscle carnitine palmitoyltransferase I (CPT I), and long-chain acyl-CoA dehydrogenase (LCAD) genes 1.7- to 3.7-fold in WG, RG, and PL muscles. Transcription rate responses were similar after 24 and 72 h of fasting. Surprisingly, increasing metabolic demand during the initial 8 h of starvation (two 2-h bouts of treadmill running) attenuated the 24-h fasting-induced transcriptional activation of UCP3, LPL, CPT I, and LCAD in RG and PL muscles, suggesting the presence of opposing regulatory mechanisms. These data demonstrate that fasting elicits a fiber type-specific coordinate increase in the transcription rate of several genes involved in and/or required for lipid metabolism and indicate that exercise may attenuate the fasting-induced transcriptional activation of specific metabolic genes.

Animals↗
PubMed1983

Interorgan relationships of alanine and glutamine during fasting in the conscious dog.

This study was designed to assess the interorgan relationships of glutamine and alanine in the conscious, overnight fasted dog, and to determine changes which occur with progressive fasting. Dogs were fasted for 18 hr (n = 6), 48 hr (n = 6), and 96 hr (n = 6) prior to the study. Catheters had been previously implanted in the femoral artery, renal vein, portal vein, and hepatic vein, and were used for blood sampling at 30-min intervals during the 3-hr experimental period. Hepatic and renal blood flows were determined by indocyanine green and para-aminohippuric acid (PAH) extraction methods, respectively. Balance data (micromoles/kilogram/minute) were estimated by multiplying the appropriate arteriovenous concentration differences by blood flows. Hepatic uptake of glutamine decreased 50% after a 48-hr fast, and by 96 hr, the liver became a net producer of glutamine. Gut utilization remained constant throughout fasting. The kidney's utilization gradually increased with fasting. The hepatic extraction of alanine fell with fasting, declining to 40% of its original uptake at 96 hr. The gut's production of alanine fell during the first 48 hr of fasting, but remained stable thereafter. The kidney's production of alanine increased throughout the period of starvation. The arterial concentration of glutamine rose with fasting, while that of alanine fell even with a 48 hr fast. The liver, by becoming a net producer of glutamine, and the kidney, by increasing its production of alanine, decrease demands for peripheral release of these two amino acids, and thus may have protein-sparing actions during fasting.

Alanine↗
PubMed1995

Effect of fasting and growth hormone (GH) administration on GH receptor (GHR) messenger ribonucleic acid (mRNA) and GH-binding protein (GHBP) mRNA levels in male rats.

To elucidate whether GHR and GHBP are coordinately regulated or not, we studied the effect of fasting with or without GH administration on the GHR and GHBP mRNAs in the liver as well as in extrahepatic tissues in rats. Tissues were collected from 7-week-old male rats by decapitation 1,3, and 7 days after the start of fasting. Liver GHR mRNA levels were not affected 1 day after the start of fasting but progressively decreased for the subsequent 3 and 7 days of fasting as compared with those in control rats fed ad libitum. In contrast, liver GHBP mRNA levels significantly rose after 1 day fasting, returned to the control level after 3 days and further reduced after 7 days of fasting. Changes in GHBP mRNA level after fasting were different among the tissues. A transient increase in GHBP mRNA levels was observed in muscle and heart as well as liver, while the GHBP mRNA levels in fat tissues did not change throughout 7 days of fasting. Next, bovine GH(bGH) was administered ip to the fasted rats and control fed rats for either 1 day(100 micrograms [corrected], tid) or 5 days(150 micrograms [corrected], daily). In fed rats, liver GHR mRNA level was significantly increased by 1 day bGH treatment, but after 5 days treatment with bGH it was not different from the level in saline-injected control. Accordingly, net increment of plasma IGF-I was 296.0 ng/ml with 1 day bGH treatment and 234.2 ng/ml with bGH administration for 5 days. In fasted rats, liver GHR mRNA level did not changed after 1 day treatment with bGH, but markedly decreased 5 days after bGH administration. Net increment of plasma IGF-I was slightly reduced to 284 ng/ml with 1 day treatment with bGH, and markedly decreased to 37.0 with bGH administration for 5 days. The effect of GH administration on liver GHBP mRNA level was virtually absent in either fasting or fed state. These findings suggest that GHR and GHBP mRNAs in the liver are expressed in different ways and that expression of GHBP mRNA is differently regulated among tissues.

Animals↗
PubMed1990

Effects of fasting on cadmium toxicity, glutathione metabolism, and metallothionein synthesis in rats.

Acute oral toxicity of Cd (as cadmium chloride) was enhanced in rats fasted 24 hr, as shown by a markedly decreased LD50. To examine the relationship among Cd toxicity, hepatic glutathione (GSH), and metallothionein (MT) during fasting, rats were administered 75 mg Cd/kg orally 24 hr after fasting and euthanized after a further 4 or 24 hr for various assays. Serum glutamic-pyruvic transaminase activity 24 hr after Cd treatment was higher in fasted rats than in fed rats. Both total GSH and nonprotein sulfhydryl (NPSH) concentrations in liver decreased to 50% of control levels after 28 hr of fasting and returned to 75% of control values by 48 hr. Total hepatic GSH concentration in fed rats decreased 4 and 24 hr after Cd treatment, whereas that in fasted rats remained unchanged at 4 hr and decreased significantly at 24 hr. Cd uptake by the liver (both concentration and content) 24 hr after Cd treatment was higher in fasted rats than in fed rats. Hepatic MT concentration was markedly increased by Cd treatment and higher in fasted rats than in fed rats. There was no relationship between Cd toxicity and hepatic thiobarbituric acid (TBA) value, an indicator of lipid peroxidation. Fasting had no effect on hepatic GSH peroxidase and GSH reductase activities. These enzymes probably are not involved in Cd toxicity. On histological examination, focal degenerative and necrotic changes were observed from the midlobular to the pericentral region in the livers of fed rats 24 hr after Cd treatment. These changes were enhanced by fasting, diffusing from the pericentral to the periportal region. Histochemical examination revealed a heterogeneous distribution of GSH in the livers of fed rats, with strong staining of GSH in the periportal region. This heterogeneous distribution of GSH in liver was not observed in fed rats 4 hr after Cd treatment or in fasted rats at 24 hr. The present results suggest that hepatic GSH plays an important role in protection against Cd toxicity before the onset of MT synthesis. Animals in bad condition, such as that resulting from interruption of nutrient supply, cannot be protected against Cd toxicity even if the hepatic MT level is high.

Animals↗
PubMed1993

Effects of valproate and E-2-en-valproate on functional and morphological parameters of rat liver. III. Influence of fasting.

Valproate (VPA) therapy has been associated with a rare but fatal hepatotoxicity. Several possible biochemical mechanisms responsible for the hepatotoxicity have been proposed, but the matter has not been decided. There is some evidence that VPA-associated hepatotoxicity may represent the consequences of a VPA overload on a limited mitochondrial beta-oxidation capacity, causing abnormalities in metabolic pathways. If this assumption is true, fasting-induced increase of endogenous fatty acids, which compete with VPA for beta-oxidation, should enhance the hepatotoxic potential of VPA. Indeed, involuntary fasting because of anorexia, e.g., in children with febrile infections, has been discussed as one clinical risk pattern preceding VPA-associated hepatic fatalities. In the present experiments, the effects of fasting on functional and morphological parameters of the liver were studied in young male rats chronically treated with VPA. E-2-en-VPA (trans-2-en-VPA), a major active metabolite of the beta-oxidation pathway of VPA, was used for comparison. Both drugs were administered at doses of 250 mg/kg i.p. 3 times daily for 1 week. In control rats, a 40-h fasting period resulted in marked mobilization of liver lipid and glycogen stores, alterations in liver enzyme activities, and hyperammonemia. In rats treated with VPA, fasting reduced beta-oxidation of the drug, but seemed not to increase its hepatotoxic potential. Compared to experiments without fasting, alterations in liver enzymes and ammonia levels induced by VPA were less marked or absent in fasted rats, and histopathological examination of liver sections did not indicate degenerative liver lesions in response to drug treatment. Thus, compared to previous rat studies on VPA without fasting, fasting appeared to attenuate VPA's hepatotoxic potency, possibly as a result of fasting-induced increases in carnitine levels. In rats treated with E-2-en-VPA, no indication of hepatotoxicity was evident, and alterations in functional hepatic parameters were less pronounced than with VPA. The data do not indicate that fasting or poor nutrition are risk factors for VPA-associated hepatic injury.

Animals↗
PubMed2004

Dietary restriction: effects of short-term fasting on protein uptake and cell death/proliferation in the rat liver.

Dietary restriction (DR) is known to prolong life in laboratory animals. Intermittent (alternate-day) fasting or short-term repeated fasting has also been reported to increase the life span of animals. In the present study, we investigated the changes or induction of abnormalities of protein metabolism in rats during fasting, and measured asialoglycoprotein uptake and cell death/proliferation in the liver of rats receiving fasting and refeeding. In the results, liver weight decreased significantly after 48 h of fasting and increased during the refeeding period, returning to the pre-fasting level by 12 h of refeeding. Cell death, determined by single stranded DNA (ssDNA) staining method, increased during the fasting period, and returned to the pre-fasting level during the refeeding period. Cell proliferation, determined using antibodies (Ab) against proliferating cell nuclear antigen, decreased during the fasting period, and increased during the refeeding period. Changes in cell death and cell proliferation were inversely related. However, there was no significant difference in asialoglycoprotein uptake by the whole liver between the ad libitum (AL)-fed rats and 48 h fasted rats. Thus, neither the changes in liver weight nor cell death/proliferation affected asialoglycoprotein uptake on a living body. These results suggest that episodes of 48 h fasting do not induce protein metabolism abnormalities in the liver.

Animals↗
PubMed1997

Effect of age on the activity of phosphoenolpyruvate carboxykinase in the kidney following fasting and refeeding.

The activity of renal phosphoenolpyruvate carboxykinase (PEPCK) was measured in 3-18 month old male Fischer 344 rats after alternate periods of fasting and refeeding. To compare the induction of renal PEPCK activity in response to fasting in young and old rats, 3, 6, 12 and 18 month old animals were fasted for 30 h followed by a 24 h ad libitum refeeding period to reduce PEPCK activity toward basal levels. The refeeding period was followed by a second 24 h fasting period during which the time course of PEPCK induction was monitored in the young and old animals. The first fast resulted in over a 20% increase in renal PEPCK activity in the 3 month old and slightly over a 70% increase in the 6 month old animals. In contrast, the activity did not increase significantly in the 12 or 18 month old animals during this fasting period. Therefore the induction of PEPCK in the kidney in response to fasting appears to be altered in the older animals. Refeeding for 24 h resulted in a decrease in PEPCK activity in all four age groups; therefore there was no indication of an age-related impairment in the response of renal PEPCK to refeeding. After the refeeding period, the food was removed again and the activity was measured at short intervals over the next 24 h to determine the time course of the induction in PEPCK activity. Interestingly, during the second fast, the activity of renal PEPCK was not significantly induced in either the young or the older animals. However, the activity measured in the older 18 month rats was consistently lower during the first 12 h of the second fast as compared to the activity in the 6 month old rats. In summary, the induction of PEPCK activity in the kidney is altered with age during an initial fast; in addition, PEPCK activity is not induced in either young or old rats during a second fasting period.

Age Factors↗
PubMed2003

Fasting is a physiological stimulus of vagus-mediated enhancement of nociception in the female rat.

The vagus nerve modulates nociception by a mechanism dependent upon gonadal hormones and the adrenal medulla. In the present study we tested the hypothesis that this modulation is dynamically controlled by physiological stimulation of structures innervated by the subdiaphragmatic vagus. Specifically, food deprivation (fasting) was employed to increase activity in the subdiaphragmatic vagus, and the experiments were performed mainly in female rats because our previous observations suggested that baseline activity in the pathway is lower in females than in males. Consistent with the hypothesis, after a 48-h fast, female rats exhibited increased nociceptive behavior in the formalin test. In contrast, fasting had no effect on formalin-evoked nociceptive behavior in male rats. The fasting-induced effect on nociception appears to be mediated by the vagus nerve since it is prevented by subdiaphragmatic vagotomy. Also similar to the previously characterized vagus-mediated modulation, the effect of fasting in the female is blocked by gonadectomy or adrenal medullectomy, and hormone replacement with 17beta-estradiol in gonadectomized female rats restored the effect of fasting. Decreased glucose metabolism apparently does not play a significant role in the effect of fasting on nociception, since the effect was unchanged when 5% glucose was provided in the drinking water throughout the fasting period. On the other hand, increasing the bulk content of the stomach (without providing nutrients) by infusion of petrolatum significantly attenuated the effect of fasting during the interphase period of the formalin response, suggesting that decreased gut distention, and possibly motility, are important in fasting-induced enhancement of nociception. These results indicate that fasting is a physiological activator of the vagus-mediated pain modulation pathway. This suggests the possibility that, especially in females, natural periodic changes in gut distention and motility may control an ongoing vagus-mediated adjustment in the organism's nociceptive sensitivity.

Adrenal Medulla↗
PubMed2000

Age-dependent changes in glycosaminoglycan content in the skin of fasted rats. A possible mechanism.

It is well recognized that during fasting or aging of animals there is a decreased content of several extracellular matrix components in the skin, including glycosaminoglycans (GAGs) and decrease in biosynthesis of these macromolecules. The mechanism for the phenomena is not known. We considered skin and blood lactate as a potential candidate to control GAG metabolism in tissues. Energetic metabolism, reflected by NAD/NADH and lactate/pyruvate ratios is changed during aging or fasting and lactate inhibits at least some GAGs biosynthesis. Therefore we have compared the level of lactate and the ratios of lactate to pyruvate in the blood and skin of fasted young and fasted adult rats and correlated them with the content of skin glycosaminoglycans. It has been found that the skin of adult rats contains about 60% of GAGs found in the skin of young animals. Fasting of both groups of animals resulted in further decrease in skin GAG content. GAG content in the skin of fasted young animals was decreased by 30% while in fasted adult rats no significant differences were observed, compared to fed animals. Lactate concentration was found to be increased over 2-fold in the skin of young fasted rats, compared to young controls. The lactate concentration in adult animals was not changed during fasting, although in both cases the lactate levels were almost 3-fold higher than in young control rats. In blood, lactate concentration increased by 40% during fasting of young animals while it decreased by about 40% during fasting of adult rats. Although no differences were found in blood lactate level between young and adult rats, the ratio of lactate/pyruvate was decreased by over 2 fold in adult rats. The relative differences in mean GAG content in the skin of all experimental groups of animals were related to the similar differences in blood glucose and lactate/pyruvate ratio. Therefore not only skin lactate but also blood lactate concentrations may reflect the extent of skin GAG biosynthesis. We have noticed that increase in the ratio of skin lactate/pyruvate concentration and decrease of the ratio in the blood is accompanied by decrease in the skin GAG content. We suggest that the phenomenon may result from utilization of lactate into glucose in the Cori cycle which regulate glucose availability for GAG biosynthesis. Therefore it can be suggested that lactate may participate in inhibition of skin GAG biosynthesis and the extent of the inhibition is reflected by the ratio of lactate/pyruvate concentrations both in the skin and blood.

Aging↗
PubMed2006

Fasting: an important issue in asthma management compliance.

BACKGROUND: Fasting, neither eating nor drinking anything between dawn (sahur time) and sundown (iftar time), may have an important role in the treatment and follow-up of asthmatic patients in countries where most of the population is Muslim. OBJECTIVE: To analyze the effects of fasting on outpatient asthmatic patients. METHODS: One hundred twenty-one fasting patients were evaluated for attendance at follow-up visits, attitudes about undergoing diagnostic investigations, and opinions and practices regarding medication use during fasting. Their sources of knowledge about asthma, fasting, and medication consumption were also evaluated. RESULTS: Ninety percent of fasting patients reported no harm with respect to religion of visiting physicians while fasting. Although 96% of the patients stated that inhaled medication could be used, only 13% continued to use medication in the same manner as when they were not fasting. Most patients rearranged their medication-consumption hours. Although 96% of the patients received general information about asthma from their physicians, rates of receiving information about the fasting-medication use relationship from physicians and religious sources were similar (37% and 32%, respectively). CONCLUSION: Most Muslim asthmatic patients do not consider asthma to be a drawback to fasting, and they continue fasting by rearranging their medication consumption times. During Ramadan, patients should be questioned about this subject and should be followed up carefully for asthma control at regular visits.

Adult↗
PubMed2002

Effect of an acute fast on energy compensation and feeding behaviour in lean men and women.

AIM: Humans appear to defend against energy deficit to a greater extent than energy surplus. Severe dietary energy restriction resulting in 5-30% weight loss often leads to hyperphagia and weight regain in lean subjects. However, the period of time over which fasting is often endured in Western society are far shorter, approximately 1-2 days. This study examined how a 36 h fast effected the subsequent day's energy and nutrient intake in a group of 24 healthy, lean men and women. METHOD: Subjects underwent two 2 day treatments, termed 'fast' and 'maintenance'. During the 'fast' treatment, subjects were fed a maintenance diet on the day prior to the fast (day -1) to prevent overeating. They then consumed non-energy drinks only, from 20:00 h on day -1 to 08:00 h on day 2 (ad libitum feeding day), thus fasting for 36 h. On the 'maintenance' protocol, subjects received a maintenance diet throughout day 1. Throughout day 2 they had ad libitum access to a range of familiar foods, which were the same for both treatments. Body weight, blood glucose and respiratory quotient were used as compliance checks. Hunger was monitored on day's -1, 1 and 2 for the fast treatment only. RESULTS: On day 2, average energy intake was 10.2 vs 12.2 MJ/day (s.e.d. 1.0) on the post-maintenance and post-fast periods, respectively (P=0.049). Subjects altered feeding behaviour, in response to the fast, only at breakfast time, selecting a higher-fat meal (P<0.005). Compared to day -1, motivation to eat was elevated during the fast (P<0.05). This continued until breakfast was consumed during the re-feeding period (day 2), when values then returned to baseline. CONCLUSION: These data suggest that a 36 h fast, which generated a negative energy balance of approximately 12 MJ, did not induce a powerful, unconditioned stimulus to compensate on the subsequent day.

Adult↗
PubMed2003

Both fasting-induced leptin reduction and GH increase are blunted in Cushing's syndrome and in simple obesity.

BACKGROUND: Simple obesity and Cushing's syndrome (CS) are two clinical models of leptin hypersecretion coupled with GH hyposecretion. Fasting inhibits leptin while stimulating GH secretion in normal human subjects. OBJECTIVES: To clarify the effect of fasting on leptin and GH secretion in obesity and CS. PATIENTS AND PROTOCOL: We studied six women with CS [age 17-66 years; body mass index (BMI) 28.6 kg/m2], seven women with visceral obesity (OB; 20-41 years; BMI 42.9 kg/m2) and seven normal women (NS; 25-31 years; BMI 19.3 kg/m2). The effects of 36-h fasting on 8-h diurnal mean leptin, GH, insulin and glucose concentrations (mLEPTc, mGHc, mINSc and mGLUc) as well as on the IGF/IGFBP system were studied. RESULTS: Before fasting, mLEPTc in OB and in CS were similar and both were higher (P < 0.01) than in NS. OB and CS showed similar mGHc, which were lower (P < 0.05) than in NS. Fasting induced a reduction in mLEPTc that was significant in NS and CS (P < 0.04) but not in OB. The mLEPTc in OB and CS after fasting remained higher (P < 0.05) than in NS. After fasting, OB and CS showed no increase in mGHc, although this clearly increased (P < 0.02) in NS. IGF-I but not IGFBP-3 levels decreased in all groups (P < 0.05). Fasting reduced mINSc and mGLUc while increasing IGFBP-1 in all groups. After fasting, mINSc in OB and CS remained higher (P < 0.03) than in NS. CONCLUSIONS: Short-term fasting has less inhibitory effect on leptin and no stimulatory effect on GH secretion in patients with Cushing's syndrome as well as simple obesity. After fasting, insulin levels in hypercortisolaemic and also in obese patients remained higher than in normal subjects suggesting that hyperinsulinism could play a role in the altered response of leptin and GH to starvation in these conditions.

Adolescent↗
PubMed2002

A plasma glucose concentration below 2.5 mmol L-1 is not an appropriate criterion to end the 72-h fast.

CONTEXT: The classical end-point to terminate the 72-h fast in a patient evaluated for a hypoglycaemic disorder is the occurrence of hypoglycaemic symptoms in association with a low plasma glucose level. However, neither the symptoms nor the plasma glucose level have been exactly defined. OBJECTIVE: To determine whether a useful cut-off plasma glucose concentration as criterion to end the prolonged fast in the absence of neuroglycopenic symptoms can be defined. DESIGN: Single centre case-control study. SETTING: Tertiary referral hospital in Switzerland. SUBJECTS: The 72-h fast was prospectively performed in 23 consecutive patients (17 women and six men) following a standardized protocol between July 1999 and January 2002. All patients were referred to our clinic for evaluation of suspected hypoglycaemia. The criterion to end the fast before 72 h was defined by the occurrence of symptoms or signs typical for neuroglycopenia irrespective of plasma glucose levels. MAIN OUTCOME MEASURE: Insulin levels and insulin to plasma glucose ratios in insulinoma patients and in individuals without insulin-secreting tumours at termination of the fast and at plasma glucose levels </=2.5 mmol L-1, prior to the occurrence of neuroglycopenic symptoms. RESULTS: In seven patients, the fast was terminated before 72 h because they developed neuroglyco-penic symptoms. Insulin-secreting tumours were found and successfully removed in these seven patients. Sixteen individuals developed no neuroglycopenic symptoms throughout the 72-h fast and an insulin-secreting tumour could be excluded in these 16 patients. Five of these 16 individuals had plasma glucose levels </=2.5 mmol L-1 during the 72-h fast. Insulin levels and insulin to glucose ratios in insulinoma patients and healthy individuals overlapped during as well as at termination of the fast. Prior to the occurrence of neuroglycopenic symptoms and at venous plasma glucose </=2.5 mmol L-1, insulin to plasma glucose ratios dropped in insulinoma patients to values within the normal range on several occasions. CONCLUSIONS: Terminating the fast at plasma glucose levels </=2.5 mmol L-1 does not allow confirmation or exclusion of an insulin-secreting tumour. Thus, the occurrence of symptoms or signs typical for neuroglycopenia is the prerequisite criterion to end the fast before 72 h.

Adolescent↗
PubMed1997

Fasting-induced changes to the pharmacokinetic behaviour of albendazole and its metabolites in calves.

The influence of fasting on the bioavailability and disposition kinetics of albendazole (ABZ) and its metabolites in cattle was investigated. ABZ (10 mg/ kg) was given by intraruminal (i.r.) (Experiment 1) and intravenous (i.v.) (Experiment 2) administration to Holstein calves either fed ad libitum (control) or subjected to a 48 h fasting period (fasted group) prior to treatment. The rate of passage of digesta through the gastrointestinal (GI) tract was evaluated by measurement of cobalt faecal excretion following the oral administration of the sodium-cobalt-ethylendiamine-tetracetic acid complex to calves subjected to the feeding conditions above described. Jugular blood and abomasal fluid (via cannula) samples were collected over 120 h post-treatment; samples were analysed by high performance liquid chromatography (HPLC) for ABZ, ABZ sulphoxide (ABZSO) and ABZ sulphone (ABZSO2). Fasting the animals prior to the i.r. treatment resulted in pronounced modifications to the plasma and abomasal fluid disposition kinetics of ABZ and its metabolites. A greater extent of GI absorption with significantly higher CmaX (150%) and AUC (310%) values for ABZSO in plasma, was observed in fasted compared to fed animals following the i.r. administration of ABZ. Extended detection of ABZ metabolites resulting in significantly longer plasma t 1/2el and MRT was also obtained in fasted compared to fed calves. These results correlated with the substantially enhanced availability of ABZ and its metabolites (AUCs over 200% greater) in the abomasal fluid of the fasted animals. Fasting did not induce changes to the plasma disposition of either ABZ or its metabolites after the i.v. treatment. The digesta passage rate, measured by the amount of cobalt excreted in faeces, was significantly lower in fasted compared to animals fed ad libitum. A delayed GI transit time that decreases the rate of passage of the drug down the digestive tract, may have accounted for enhanced ABZ dissolution and absorption in fasted compared to fed calves. The findings reported in this article show that fasting prior to treatment notably affects the bioavailability and disposition kinetics of ABZ and its metabolites in cattle.

Abomasum↗