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PubMed1999

Fasting limits norepinephrine release with myocardial ischemia and reperfusion.

INTRODUCTION: Fasting for 24 hours improves functional recovery and reduces injury due to global ischemia and reperfusion. Since fasting affects catecholamine kinetics, and norepinephrine (NE) release has been implicated as a mediator of dysrhythmias and injury with myocardial ischemia, we hypothesized that fasting would limit NE release following ischemia and reperfusion as a mechanism of its beneficial effects. METHODS: Hearts were isolated and perfused from rats either fed normally or fasted for 24 hours. Following baseline perfusion, hearts were subjected to 20 minutes of ischemia followed by reperfusion. Hemodynamics (developed and end-diastolic pressure) and dysrhythmias were monitored, and creatine kinase release on reperfusion was measured as a marker of cellular injury. NE tissue content was assessed prior to ischemia and NE release was measured upon reperfusion with and without blockade of the uptake1 carrier using desipramine. RESULTS: The release of NE was reduced by fasting (0.52+/-0.14 vs. 1.47+/-0.15 nmol/gdw, p<0.001) associated with a reduction in dysrhythmias, lower creatine kinase release, and lower end-diastolic pressure on reperfusion. However, fasting did not reduce NE tissue stores prior to ischemia. Desipramine also reduced NE release on reperfusion and limited the frequency of dysrhythmias, but did not alter ischemic injury. CONCLUSIONS: Fasting limits NE release after ischemia and reperfusion, an effect not due to lower NE stores. Lower NE release, either by fasting or blockade of the uptake1, carrier, significantly reduces the frequency of dysrhythmias. However, the amount of NE release, per se, does not alter ischemic injury, suggesting that the infarct limiting effect of fasting is not mediated by lower NE release.

Adrenergic Uptake Inhibitors↗
PubMed2005

Glucose tolerance and skeletal muscle gene expression in response to alternate day fasting.

OBJECTIVE: Alternate day fasting may extend lifespan in rodents and is feasible for short periods in nonobese humans. The aim of this study was to examine the effects of 3 weeks of alternate day fasting on glucose tolerance and skeletal muscle expression of genes involved in fatty acid transport/oxidation, mitochondrial biogenesis, and stress response. RESEARCH METHODS AND PROCEDURES: Glucose and insulin responses to a standard meal were tested in nonobese subjects (eight men and eight women; BMI, 20 to 30 kg/m(2)) at baseline and after 22 days of alternate day fasting (36 hour fast). Muscle biopsies were obtained from a subset of subjects (n = 11) at baseline and on day 21 (12-hour fast). RESULTS: Glucose response to a meal was slightly impaired in women after 3 weeks of treatment (p < 0.01), but insulin response was unchanged. However, men had no change in glucose response and a significant reduction in insulin response (p < 0.03). There were no significant changes in the expression of genes involved in mitochondrial biogenesis or fatty acid transport/oxidation, although a trend toward increased CPT1 expression was observed (p < 0.08). SIRT1 mRNA expression was increased after alternate day fasting (p = 0.01). DISCUSSION: Alternate day fasting may adversely affect glucose tolerance in nonobese women but not in nonobese men. The gene expression results indicate that fatty acid oxidation and mitochondrial biogenesis are unaffected by alternate day fasting. However, the increased expression in SIRT1 suggests that alternate day fasting may improve stress resistance, a commonly observed feature of calorie-restricted rodents.

Adult↗
PubMed2001

Effects of 36 hour fasting on GH/IGF-I axis and metabolic parameters in patients with simple obesity. Comparison with normal subjects and hypopituitary patients with severe GH deficiency.

OBJECTIVE: Reduction of growth hormone (GH) secretion in obesity probably reflects neuroendocrine and metabolic abnormalities. Even short-term fasting stimulates GH secretion and distinguishes normal from hypopituitary subjects with growth hormone deficiency (GHD). Marked weight loss improves GH secretion in obesity but the effect of fasting is controversial. We studied the effects of a 36 h fasting on the GH/IGF-I axis and metabolic parameters in obesity. SUBJECTS: We studied nine obese patients (OB; three male and six female; age, 29.2+/-4.8; range, 18-59 y; body mass index (BMI), 43.4+/-2.7 kg/m(2); WHR, 0.9+/-0.1). Fifteen normal subjects (NS; eight male and seven female 28.9+/-0.6, 25-35 y; 21.6+/-0.4 kg/m(2)) and 10 adult hypopituitary patients with severe GH deficiency (GHD; seven male and three female; 37.6+/-2.3, 29-50 y; 24.5+/-1.0 kg/m(2); GH peak<3 microg/l after ITT and/or<9 microg/l after GHRH+arginine) served as control groups. STUDY DESIGN: We studied the effects of 36 h fasting on 8 h diurnal mean GH, insulin and glucose concentrations (mGHc, mINSc and mGLUc; assay every 30 min from 8.00 am to 4.00 pm) as well as on IGF-I, IGFBP-3, ALS, IGFBP-1, GHBP and free fatty acid (FFA) levels. RESULTS: Before fasting, basal IGF-I and ALS levels in OB were similar to those in NS and both were higher (P<0.001) than those in GHD. IGFBP-3 levels in OB were lower (P<0.01) than in NS but higher (P<0.02) than in GHD. GHBP levels in OB and GHD were similar and both were higher (P<0.01) than in NS. Glucose levels were similar in all groups. FFA levels in OB were higher (P<0.01) than in NS but similar to those in GHD. IGFBP-1 in OB were lower (P<0.05) than in NS and GHD which, in turn, were similar. On the other hand, mINSc in OB was higher (P<0.01) than that in NS and GHD which, in turn, were similar. The mGHc in OB was similar to that in NS but only the latter was higher (P<0.05) than in GHD. The individual mGHc in the three groups overlapped. After fasting, IGF-I levels in GHD were unchanged while they decreased in OB (P=NS) as well as in NS (P<0.01). IGFBP-3 and ALS levels did not change. GHBP levels in OB and GHD were unchanged while they increased in NS (P<0.01). Glucose and FFA levels were reduced and increased, respectively, in all groups (P<0.02 and P<0.01). IGFBP-1 increased while mINSc decreased in all groups (P<0.02 and P<0.01); in OB they persisted lower and higher (P<0.01) respectively, than in NS and GHD. Fasting significantly increased mGHc in NS (P<0.001) but not in OB as well as in GHD. Individual mGHc in OB showed persistent overlap with GHD. CONCLUSIONS: Short-term fasting does not increase GH secretion in obesity and does not distinguish somatotroph function in obese from that in severe GHD adults. Short-term fasting in obesity has attenuated effects on insulin and IGFBP-1 secretion while it normally increases free fatty acids in spite of any change in GH secretion.

Adolescent↗
PubMed2006

Effect of fasting on the pattern of urinary arsenic excretion.

Millions of people in some of the poorest regions of the world are exposed to high levels of arsenic through drinking contaminated water. It has been reported that development of cancer caused by arsenic exposure in such populations is dependent on dietary and nutritional factors which can modulate arsenic metabolism. Many people in arsenic exposed regions of Bangladesh and India practice fasting for at least one month every year when they refrain from consumption of food and fluid during daylight hours. How such practices may modulate arsenic metabolism has not been previously investigated. This study investigated this issue by determining total arsenic and its species in urine samples from a group of 29 unexposed volunteers at the beginning of the fasting and at the end of approximately 12 h of fasting period. Inductively coupled plasma mass spectrometry (ICP-MS) and high performance liquid chromatography (HPLC) coupled with ICP-MS was used to measure the total arsenic and arsenic speciation in the urine samples, respectively. The mean total levels of arsenic at the beginning of fasting (18.3 microg g(-1) creatinine) and at the end of approximately 12 h of fasting (17.7 microg g(-1) creatinine) did not differ significantly (p > 0.05). However, the percentages of urinary arsenic as the methylated arsenic species methylarsonate (MA) were found to be significantly different (p < 0.05) and this species was observed more frequently at the end of fasting, although its overall concentration was similar. There were no significant differences (p > 0.05) in both the concentrations and percentages of other urinary arsenic species detected, namely arsenobetaine (AB) and dimethylarsinate (DMA). Arsenite (As(III)) and arsenate (As(V)) were also analyzed, but were not detected. We conclude that fasting for a period of 12 h results in a significant increase in the percentage of urinary arsenic as MA, and its frequency of detection in the volunteers at the end of the fasting period is almost nine fold higher. This suggests that metabolism of arsenic is altered by fasting.

Adult↗
PubMed1995

Effects of fasting on hepatic and peripheral glucose metabolism in conscious rats with near-total fat depletion.

Experimental diabetes and fasting are both associated with hypoinsulinaemia and share several other metabolic features. We investigated hepatic and peripheral glucose metabolism in young rats after near-total depletion of their fat mass. Conscious rats were fasted for 72 h (n = 13), while 6 h-fasted animals (n = 14) served as controls. Rats were studied either during saline infusion or insulin (18 m-units/kg per min)-clamp studies. In fasting, despite a 2-fold increase in hepatic glucose-6-phosphatase (Glc-6-Pase) Vmax. (from 16 +/- 2 mumol/g of liver per min in control; P < 0.001), the basal hepatic glucose production (HGP) decreased by 47% [from 88 +/- 3 mumol/kg lean body mass (LBM) per min in control; P < 0.01]. The decreased HGP in fasting was associated with a 70% decrease in the hepatic levels of glucose 6-phosphate (Glc-6-P) (from 366 +/- 53 nmol/g wet wt. in control; P < 0.01). Thus Glc-6-Pase activity assayed in the presence of the Glc-6-P levels found in vivo was decreased by 44%. During hyperinsulinaemia, peripheral glucose uptake was decreased by 15% with 3 days of fasting (from 272 +/- 17 mumol/kg LBM per min in control; P < 0.01). This was completely accounted for by a 42% decrease in whole-body glycolysis (P < 0.01), while the rate of glycogen synthesis was unchanged. Thus fasting (after near-total fat depletion) differs from experimental diabetes because: (1) despite markedly increased Glc-6-Pase, HGP is decreased in fasting, due to a marked decrease in the substrate level (Glc-6-P) in vivo; and (2) the impairment in peripheral insulin sensitivity in fasting is due to a decrease in the glycolytic, and not the glycogen-synthetic, pathway.

Animals↗
PubMed2000

Fasting induces impairment of gastric mucosal integrity in non-insulin-dependent diabetic (db/db) mice.

BACKGROUND: Although diabetic patients often have gastrointestinal complications, the gastric mucosal function in diabetes has not been well documented. AIM: To investigate the effect of fasting on the gastric mucosa in C57BL/KsJ-db +/+ db (db/db) mice, genetically non-insulin-dependent diabetic animals. METHODS: Blood glucose levels, gastric mucosal morphology, and the amount of gastric mucin were examined before and after 18 h of fasting with free access to water in db/db mice and their non-diabetic littermates (db/m). RESULTS: Although 18 h of fasting reduced the blood glucose levels of both db/db and db/m mice, fasting decreased the amount of gastric adherent mucin and caused haemorrhagic gastric lesions only in db/db mice. After fasting, oral administration of ethanol induced much more severe gastric damage in db/db than in db/m mice. The above fasting-induced gastric damage such as haemorrhagic lesions, loss of the mucin, and the increased sensitivity to ethanol worsened as the duration of diabetes became longer. Glucose ingestion in drinking water during the fasting counteracted the fall in blood glucose and prevented the decrease in the amount of gastric mucin and the formation of gastric mucosal lesions in db/db mice. CONCLUSION: These findings indicate that fasting-induced glucose deficit causes gastric mucosal lesions and increases the susceptibility of gastric mucosa to noxious agents owing to the loss of mucus glycoprotein in db/db mice. Prolonged diabetes is likely to augment the severity of fasting-induced impairment of the gastric mucosal function.

Aging↗
PubMed2001

Attitudes and practices of breastfeeding mothers regarding fasting in Ramadan.

OBJECTIVE: To investigate the attitudes and practices of breastfeeding mothers regarding fasting in Ramadan. DESIGN: Cross-sectional observational survey. SETTING: Well-child care clinic at Ankara University Medical School and a health station serving an impoverished population in Ankara, Turkey. PARTICIPANTS: Breastfeeding mothers of infants aged 12 months or younger. MAIN OUTCOME MEASURES: Fasting during Ramadan. RESULTS: Of the 164 participating mothers, 61 (37%) were from the health station and 103 (63%) from the university clinic. Most mothers were older than 25 years of age (55%), had more than primary school education (64%), a single child (53%), were living in a nuclear family setting (70%), supplementing breastfeeding (73%) and fasting (52%). Among the 129 mothers of infants aged 6 months or younger, 22% perceived a decrease in their breast milk and 23% an increase in the amount of solid supplements the infant was receiving. Belief that breastfeeding mothers should fast (RR = 6.45, 95% CI: 2.44-17.06), that fasting does not decrease breast milk (RR = 6.24, 95% CI: 1.85-21.05), receiving well-child care at the health station (RR = 3.14, 95% CI: 1.33-7.44), giving supplements (RR = 2.82, 95% CI: 1.09-7.27) and having multiple children (RR = 2.78, 95% CI: 1.23-6.28) were associated with fasting, in a logistic regression model. CONCLUSIONS: Fasting by breastfeeding mothers of infants is common during Ramadan, and rates are affected by beliefs of mothers on the effects of fasting on breastfeeding. We believe that child health care providers need to be knowledgeable about religious and cultural phenomena, study the effects of Ramadan fasting and form links with Islamic teachings to find religiously and culturally appropriate methods to combat the possible unfavourable effects for infants and children.

Adult↗
PubMed2001

Effects of fasting and pegvisomant on the GH-releasing hormone and GH-releasing peptide-6 stimulated growth hormone secretion.

OBJECTIVE: Pegvisomant is a mutated GH molecule which prevents functional dimerization and subsequent activation of the growth hormone receptor. Pegvisomant and fasting both lead to GH resistance. DESIGN AND PATIENTS: We performed a double-blind placebo-controlled cross-over study comparing the effects of pegvisomant and fasting on the GH-releasing hormone (GHRH)- and GH-releasing peptide-6 (GHRP-6)-stimulated GH-release before and after 3 days of fasting in 10 healthy lean male subjects. We also performed a single-arm open label study under nonfasting conditions in five of these subjects. On day 1, in random order, at 0800 h, a GHRP-6 or GHRH test was performed. At 1600 h, a GHRH (if the first test was a GHRP-6 test) or GHRP-6-test (if the first test was a GHRH test) was done. After the second test either pegvisomant (80 mg as a single subcutaneous injection) or placebo was administered. On day 4, GHRP-6 and GHRH tests were performed in the same order as on day 1. During the cross-over study, subjects fasted from 2400 h on day 1 until the end of the study. MEASUREMENTS: During the GH stimulation tests, blood samples were drawn every 15 min from 15 to 120 min. GH was determined in all samples. Total insulin-like growth factor (IGF)-I and free IGF-I were determined from the samples at 0 min only. RESULTS: Three days of fasting alone and pegvisomant alone as well as in combination increased GH concentrations, whereas a decrease in serum-free, but not total, IGF-I concentrations was observed. On day 4, fasting and pegvisomant, either alone or in combination, significantly increased GH concentrations after GHRH compared to baseline. Pegvisomant alone did not increase GH concentrations after GHRP-6 administration. Fasting alone increased GH levels after GHRP-6 administration. The combination of fasting and pegvisomant had a synergistic effect on GH release after GHRP-6. CONCLUSION: These human in vivo data suggest that: (1) circulating free IGF-I, and not total IGF-I, is the major component in the negative feedback on GH secretion; (2) increased pituitary GHRH receptor expression plays a role in the mechanism whereby fasting leads to increased GH concentrations; (3) in vivo, GHRP-6 sensitivity seems to be regulated primarily by metabolic factors and not by changes in GH-IGF-I axis.

Adult↗
PubMed2001

Differential effects of fasting and dehydration in the pathogenesis of diabetic ketoacidosis.

Glycemia varies widely in patients with diabetic ketoacidosis (DKA), with plasma glucose concentrations between 10 to 50 mmol/L commonly encountered. The mechanism of this glycemic variability is uncertain. Our study examined the differential effects of fasting and dehydration on hyperglycemia induced by withdrawal of insulin in type 1 diabetes. To evaluate the respective roles of dehydration and fasting in the pathogenesis of DKA, 25 subjects with type 1 diabetes were studied during 5 hours of insulin withdrawal before (control) and after either 32 hours of fasting (n = 10) or dehydration of 4.1% +/- 2.0% of baseline body weight (n = 15). Samples were obtained every 30 minutes during insulin withdrawal for substrate and counterregulatory hormone levels and rates of glucose production and disposal. Fasting resulted in reduced plasma glucose concentrations compared with the control study, while dehydration resulted in increased plasma glucose concentrations compared with the control study (P < .001). Glucose production and disposal were decreased during the fasting study and increased during the dehydration study compared with the control study. Glucagon concentrations and rates of development of ketosis and metabolic acidosis were increased during both fasting and dehydration compared with control. These data suggest that fasting and dehydration have differential effects on glycemia during insulin deficiency, with dehydration favoring the development of hyperglycemia and fasting resulting in reduced glucose concentrations. This finding is probably attributable to the differing effect of these conditions on endogenous glucose production, as well as to differences in substrate availability and counterregulatory hormone concentrations. The severity of pre-existing fasting and dehydration likely explains much of the variability in plasma glucose concentrations observed in DKA.

Adult↗
PubMed2001

Insulin sensitivity measured by the minimal model: no associations with fasting respiratory exchange ratio in trained athletes.

The aim of this study was to examine the role of fasting insulin concentrations and tissue insulin sensitivity on whole-body substrate oxidation in 61 well-trained subjects. Subjects underwent a frequently sampled intravenous glucose tolerance test (FSIVGT) after a 10- to 12-hour overnight fast. Minimal model analysis was used to determine insulin sensitivity (S(i)). A week later, fasting (10- to 12-hour) respiratory exchange ratio (RER) was measured at rest and during exercise at 25%, 50%, and 70% of peak power output (W(peak)). Prior to these measurements, training volume, dietary intake, and muscle fiber composition, substrate concentrations, and enzyme activities were determined. The average fasting plasma insulin concentration was 7.3 +/- 2.4 microU/mL (4.0 to 10.5 microU/mL), and the mean S(i) was 14.0 +/- 6.1 x (10(-4) min(-1) x microU(-1) x mL(-1)) (2.6 to 26.3 x 10(-4) min(-1) x microU(-1) x mL(-1)). There was no significant correlation between fasting plasma insulin concentration and S(i) (r = -.14, P =.336) or between these measurements and fasting RER, measured at rest and during exercise at 25%, 50%, and 70% W(peak). Only VO(2max) and the proportion of type 1 muscle fibers were significantly correlated with S(i) (r =.30, P =.045 and r =.34, P =.026, respectively), and waist-to-hip ratio (WHR) was significantly correlated with fasting plasma insulin concentration (r =.35, P =.006). In conclusion, S(i) and fasting plasma insulin concentration were not associated with fasting RER at rest and during exercise of increasing intensity in trained athletes who have high S(i).

Adult↗
PubMed1983

Effect of fasting on posthyperglycemic glucose homeostasis in obesity--experimental model for reactive hypoglycemia.

The relationship between altered glucose-insulin interaction in the hyperglycemic period of oral glucose tolerance test (oGTT) and impaired posthyperglycemic glucose homeostasis was studied in 9 obese females. They underwent 6-hour oGTT following 72-96 hour total fast, and the results of blood glucose, insulin, growth hormone, cortisol, glucagon and free fatty acids were compared to those of the control test. Blood glucose values in the hyperglycemic period of oGTT were higher during the post-fasting than in the control study. Posthyperglycemic glucose levels following fast dropped below the control values and four patients showed subjective symptoms of reactive hypoglycemia. Mean maximum blood glucose irrespective of time was significantly higher, mean glucose nadir lower after fast than in the control experiment (138.4 +/- 7.1 mg/dl vs. 112.4 +/- 5.2 and 47.3 +/- 1.4 vs. 61.3 +/- 3.0, respectively). Insulin response following fast was significantly reduced in 0-2 h period with delayed maximum value obtained at 123.3 +/- 14.5 min vs. 60.0 +/- 10.0 min in the basal experiment. Post-fasting counter-regulatory cortisol response was higher when compared to control, but there was no difference in growth hormone and glucagon secretion. Basal and post-glucose values of free fatty acids were significantly higher after fast than in the control study. The data suggest that fasting-induced impairment of glucose-insulin interaction in the hyperglycemic period of oGTT decreases the ability of obese subjects to maintain posthyperglycemic glucose homeostasis and provokes reactive hypoglycemia in some of them. Examination of glucose metabolism in fasted subjects is a convenient experimental model for the investigation of reactive hypoglycemia.

Blood Glucose↗
PubMed2004

Short-term fasting and lipolytic activity in rat adipocytes.

The aim of this experiment was to study the influence of 18-hour food deprivation on basal and stimulated lipolysis in adipocytes obtained from young male Wistar rats. Fat cells from fed and fasted rats were isolated from the epididymal adipose tissue by collagenase digestion. Adipocytes were incubated in Krebs-Ringer buffer (pH 7.4, 37 degrees C) without agents affecting lipolysis and with different lipolytic stimulators (epinephrine, forskolin, dibutyryl-cAMP, theophylline, DPCPX, amrinone) or inhibitors (PIA, H-89, insulin). After 60 min of incubation, glycerol and, in some cases, also fatty acids released from adipocytes to the incubation medium were determined. Basal lipolysis was substantially potentiated in cells of fasted rats in comparison to adipocytes isolated from fed animals. The inhibition of protein kinase A activity by H-89 partially suppressed lipolysis in both groups of adipocytes, but did not eliminate this difference. The agonist of adenosine A (1) receptor also did not suppress fasting-enhanced basal lipolysis. The epinephrine-induced triglyceride breakdown was also enhanced by fasting. Similarly, the direct activation of adenylyl cyclase by forskolin or protein kinase A by dibutyryl-cAMP resulted in a higher lipolytic response in cells derived from fasted animals. These results indicate that the fasting-induced rise in lipolysis results predominantly from changes in the lipolytic cascade downstream from protein kinase A. The antagonism of the adenosine A (1) receptor and the inhibition of cAMP phosphodiesterase also induced lipolysis, which was potentiated by food deprivation. Moreover, the rise in basal and epinephrine-stimulated lipolysis in adipocytes of fasted rats was shown to be associated with a diminished non-esterified fatty acids/glycerol molar ratio. This effect was presumably due to increased re-esterification of triglyceride-derived fatty acids in cells of fasted rats. Comparing fed and fasted rats for the antilipolytic effect of insulin in adipocytes revealed that short-term food deprivation resulted in a substantial deterioration of the ability of insulin to suppress epinephrine-induced lipolysis.

Adipocytes↗
PubMed2006

Assessment of basal insulin requirement using fasting tests in insulin-treated patients with type 2 diabetes mellitus.

AIMS: Characterizing the time course of the rise of blood glucose concentrations in the fasting state during the day and night in patients with type 2 diabetes. METHODS: 40 consecutive insulin-treated patients with type 2 diabetes underwent fasting tests on two different days with either no breakfast and lunch (fasting time of 20 hours) or no dinner (fasting time of 21 hours). Glucose-lowering medication was stopped prior to the test according to the half-life of the medication prescribed. At the start of the fasting tests, blood glucose concentrations were lowered to below 7 mmol/L using an insulin infusion. RESULTS: 26 men and 14 women were included in the study. Mean (+/-SD) age was 61+/-10 years, BMI 31+/-7 kg/m (2), and HbA1c 7.5+/-1%. Diabetes duration was 14+/-8 years and duration of insulin therapy had been prescribed for a mean of 6+/-6 years. During the daytime fast, plasma glucose concentrations rose by a mean of 0.8+/-1.6 mmol/L. During the nighttime fast, plasma glucose concentrations increased particularly after midnight, by 4.3+/-2.1 mmol/L, i.e. significantly more than during the daytime fast. CONCLUSIONS: Fasting blood glucose concentrations in the majority of insulin-treated patients with type 2 diabetes increase markedly after midnight. No similar increase is observed during the day. Thus, for most patients with type 2 diabetes, an intermediate- or long-acting insulin injected at bedtime with a peak action six to eight hours after injection should be appropriate.

Aged↗
PubMed1993

Evidence for increased sensitivity of fuel mobilization to growth hormone during short-term fasting in humans.

Since growth hormone (GH) secretion is increased with fasting, the study was designed to assess the effects of short-term fasting on both basal and GH stimulated substrate metabolism. Seven normal healthy subjects were studied following a 12 h and a 36 h fast ("fasting"), for 2 h in the basal state and for a further 4 1/2 h after an i.v. bolus injection of 140 micrograms GH. As expected fasting induced decrements in circulating concentrations of insulin and C-peptide (p < 0.05) and increments in glucagon concentrations (p < 0.05), together with a slight increase in serum GH concentrations (p > 0.05). Furthermore plasma glucose values, isotopically determined turnover rate for glucose and forearm uptake of glucose were all substantially reduced during fasting (p < 0.05). By contrast circulating levels of all measured lipid intermediates (free fatty acids [FFA], 3-hydroxybutyrate [3-OHB] and glycerol) and the forearm uptake of 3-OHB were clearly elevated during the fast (p < 0.05). Serum GH rose to a peak of 17.0 +/- 2.7 within 10 min of injection in both situations. Blood concentrations of hormones and parameters of glucose metabolism remained unaffected. After administration of GH circulating levels of lipid intermediates increased markedly in both situations, the increase being most pronounced in the fasting state (p < 0.05). During fasting peak levels of 1775 +/- 150 mumol/l and 1780 +/- 360 mumol/l of FFA and 3-OHB were observed compared to postabsorptive peaks of 980 +/- 100 and 230 +/- 90 mumol/l respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Normal fasting plasma glucose levels and type 2 diabetes in young men.

BACKGROUND: The normal fasting plasma glucose level was recently defined as less than 100 mg per deciliter (5.55 mmol per liter). Whether higher fasting plasma glucose levels within this range independently predict type 2 diabetes in young adults is unclear. METHODS: We obtained blood measurements, data from physical examinations, and medical and lifestyle information from men in the Israel Defense Forces who were 26 to 45 years of age. RESULTS: A total of 208 incident cases of type 2 diabetes occurred during 74,309 person-years of follow-up (from 1992 through 2004) among 13,163 subjects who had baseline fasting plasma glucose levels of less than 100 mg per deciliter. A multivariate model, adjusted for age, family history of diabetes, body-mass index, physical-activity level, smoking status, and serum triglyceride levels, revealed a progressively increased risk of type 2 diabetes in men with fasting plasma glucose levels of 87 mg per deciliter (4.83 mmol per liter) or more, as compared with those whose levels were in the bottom quintile (less than 81 mg per deciliter [4.5 mmol per liter], P for trend <0.001). In multivariate models, men with serum triglyceride levels of 150 mg per deciliter (1.69 mmol per liter) or more, combined with fasting plasma glucose levels of 91 to 99 mg per deciliter (5.05 to 5.50 mmol per liter), had a hazard ratio of 8.23 (95 percent confidence interval, 3.6 to 19.0) for diabetes, as compared with men with a combined triglyceride level of less than 150 mg per deciliter and fasting glucose levels of less than 86 mg per deciliter (4.77 mmol per liter). The joint effect of a body-mass index (the weight in kilograms divided by the square of the height in meters) of 30 or more and a fasting plasma glucose level of 91 to 99 mg per deciliter resulted in a hazard ratio of 8.29 (95 percent confidence interval, 3.8 to 17.8), as compared with a body-mass index of less than 25 and a fasting plasma glucose level of less than 86 mg per deciliter. CONCLUSIONS: Higher fasting plasma glucose levels within the normoglycemic range constitute an independent risk factor for type 2 diabetes among young men, and such levels may help, along with body-mass index and triglyceride levels, to identify apparently healthy men at increased risk for diabetes.

Adult↗
PubMed1997

Effects of fasting, hypoxia, methylpalmoxirate and oxfenicine on the tissue-levels of long-chain acyl CoA and acylcarnitine in the rat atria.

During hypoxia the atria from fasted rats exhibit a faster decline in the pacemaker and contractile activities than those from fed rats. Oxfenicine and methylpalmoxirate, inhibitors of carnitine palmitoyltransferase 1 (CPT 1), ameliorate these disturbances. Since the fasted rat atria have greater triacylglycerol stores and a faster lipolysis, and CPT 1 funnels fatty acid into beta-oxidation, the effects of fasting could be ascribed to the accumulation of amphipathic metabolites such as long-chain acyl CoA (LCCoA) and long-chain acylcarnitine (LCCa). Hence, this investigation aimed to assess whether the levels of these metabolites correlate with the effects of fasting and CPT 1 inhibitors. At the end of the prehypoxic equilibration period the fasted rat atria had a 6.5-fold greater content of LCCa than those of the fed rats and methylpalmoxirate impeded the increase. During hypoxia the LCCoA content increased 9-fold in the fasted rat atria, LCCa levels were 3.6-fold greater in the fasted than in the fed group, and free-CoA and free-carnitine showed a significant fall. The increases of LCCoA and LCCa as well as the fall in free-CoA were abolished by both inhibitors. The decrease of free-carnitine was impeded by methylpalmoxirate, but oxfenicine unexpectedly decreased its concentration in both nutritional groups. These data suggest that: (1) the atrial CPT 1 activity is enhanced during fasting, (2) in the hypoxic atria levels of LCCoA and LCCa were closely correlated with the noxious effects of fasting and the amelioration effected by CPT 1 inhibitors, and (3) the effects of amphipathic metabolites during oxygen deprivation can be attenuated by pharmacological interventions.

Acyl Coenzyme A↗
PubMed1983

Blood flow and nutrient exchange across the liver and gut of the dairy cow. Effects of lactation and fasting.

The rate of blood flow in the portal and hepatic veins, and the net exchange across the gut and liver of volatile fatty acids (VFA), glucose, lactate, pyruvate, amino acids, ketone bodies, glycerol, non-esterified fatty acids (NEFA) and oxygen, were measured in lactating and non-lactating cows (a) in the normal, fed state and (b) before, during and after 6 d of fasting. Blood flow rate through the liver was 52% higher in normal, fed, lactating cows as compared with non-lactating cows, and was decreased by fasting in both groups of cows. Portal blood flow rate increased with an increase in metabolizable energy (ME) intake. Lactating, as compared with non-lactating, cows exhibited lower arterial concentrations of glucose and lactate, higher net portal outputs of VFA and ketone bodies, a higher net hepatic output of glucose, and higher net hepatic uptake of propionate and lactate. The splanchnic outputs of acetate, glucose and hydroxybutyrate were all apparently greater in the lactating cows. Fasting caused a rapid decrease in the blood concentrations of the VFA and an increase in those of glycerol and NEFA. The portal, i.e. gut, outputs of VFA, lactate, ketone bodies, alanine and (serine + threonine), and the portal uptake of O2, were all decreased by fasting. Fasting for 6 h also decreased the hepatic output of glucose and acetate by 77 and 95% respectively, increased the hepatic uptake of pyruvate, glycerol and NEFA, and doubled hepatic ketone-body output. The splanchnic output of acetate and glucose and the splanchnic uptake of O2 were also decreased by fasting. The net portal outputs of VFA, lactate and hydroxybutyrate, and the net hepatic output of glucose, were all correlated with ME intake in fed and fasted cows. Hepatic glucose output was also correlated with milk yield. The net hepatic uptake of gluconeogenic precursors measured in this study could account for net hepatic glucose output in the fasted cows, but not in the fed cows. The net hepatic uptake of the ketogenic precursors butyrate and NEFA was sufficient to account for the hepatic output of ketone bodies in both fed and fasted cows, but it is unlikely that the hepatic uptake of ketogenic precursors could also account for the observed hepatic output of acetate.

Amino Acids↗
PubMed2006

Influence of fasting on the effects of dimethylamiloride and oxfenicine on ischaemic-reperfused rat hearts.

To assess whether glycolysis, Na+-H+ exchange and oxidation of fatty acid derived from endogenous lipolysis are involved in the beneficial effects of 24-h fasting on the ischaemic - reperfused heart, it was studied the effects of inhibiting Na+ - H+ exchange using 10 muM dimethylamiloride and fatty acid oxidation using 2 mM oxfenicine, on the functional activity, lactate production and cell viability measured with tetrazolium stain. Since fasting accelerates heart fatty acid oxidation, data were compared to those from fed rats; using Langendorff perfused (glucose 10 mM) hearts of 250-350 g Wistar rats exposed to 25 min ischaemia - 30 min reperfusion. Fasting reduced the ischaemic rise of end diastolic pressure (contracture), improved recovery of contraction and lowered lactate production in comparison with the fed whereas cellular viability was similar in both groups. Dimethylamiloride improved the recovery of contraction (fed control 24 +/- 9%, fed treated 68 +/- 11%, P < 0.05 at the end of reperfusion), attenuated the contracture (fed control 40 +/- 9%, fed treated 24 +/- 11%, P < 0.05 at the beginning of reperfusion) and reduced lactate production in the fed group and increased cellular viability in both groups (fed control 21 +/- 6%, fed treated 69 +/- 7%, P < 0.05, and fasted control 18 +/- 7%, fasted treated 53 +/- 8%, P < 0.05). Oxfenicine reduced the recovery of contraction (fasted control 88 +/- 6%, fasted treated 60 +/- 11%, P < 0.05) and increased lactate production of fasted group and attenuated the contracture in the fed. These data suggest that beneficial effects of fasting owe, at least in part, to a lowered glycolysis probably secondary to the increased fatty acid oxidation and to the accumulation of energy supplying acyl esters. Dimethylamiloride slowing of glycolysis might explain functional improvement, whereas it seems unrelated to the protection on cell viability.

Amiloride↗