Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FASTING”

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

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

At least 559 records · Page 31Linked to original sources
PubMed2003

Effects of a brisk walk on lipoprotein lipase activity and plasma triglyceride concentrations in the fasted and postprandial states.

This study aimed to determine whether changes in plasma heparin-releasable lipoprotein lipase (LPL) activity following a brisk walk were associated with decreases in fasting and/or postprandial triglyceride (TG) concentrations. Two groups of pre-menopausal women participated. In one group (fasting study group, n=10), TG concentrations and post-heparin plasma LPL activity were measured in the fasted state on two occasions: approximately 18 h after a 2-h treadmill walk at 50% maximal oxygen uptake (exercise trial); and after a day of no exercise (control trial). The other group (postprandial study group, n=9) undertook two oral fat tolerance tests (blood samples taken fasting and for 6 h after a high-fat meal), with plasma LPL activity measured 6 h after meal ingestion. Pre-conditions were the same as for the fasting study group (i.e. control and prior exercise). Prior exercise reduced fasting TG concentrations by 23 (7)% (fasting study group) [mean (SEM)] and by 18 (9)% (postprandial study group) (both P<0.05), and the postprandial TG response by 23 (6)% (postprandial study group) (P<0.01). Plasma LPL activity was not significantly increased by exercise in either the fasting or postprandial study groups. However, exercise-induced changes in both fasting and postprandial LPL activity were significantly correlated with the respective exercise-induced changes in fasting TG concentration and the postprandial TG response (r=-0.70 and -0.77 respectively, P<0.05 for both). These data suggest that increased LPL activity may contribute to the hypotriglyceridaemic effect of moderate exercise, although other mechanisms are also likely to be involved.

Adult↗
PubMed2002

Skeletal muscle heterogeneity in fasting-induced upregulation of genes encoding UCP2, UCP3, PPARgamma and key enzymes of lipid oxidation.

The uncoupling protein homologs UCP2 and UCP3 have been proposed as candidate genes for the regulation of lipid metabolism. Within the context of this hypothesis, we have compared, from fed and fasted rats, changes in gene expression of skeletal muscle UCP2 and UCP3 with those of carnitine palmitoyltransferase I and medium-chain acyl-CoA dehydrogenase, two key enzymes regulating lipid flux across the mitochondrial beta-oxidation pathway. In addition, changes in gene expression of peroxisome proliferator-activated receptor gamma, a nuclear transcription factor implicated in lipid metabolism, were also investigated. The results indicate that in response to fasting, the mRNA levels of UCP2, UCP3, carnitine palmitoyltransferase I and medium-chain acyl-CoA dehydrogenase are markedly increased, by three- to sevenfold, in the gastrocnemius and tibialis anterior (fast-twitch muscles, predominantly glycolytic or oxidative-glycolytic), but only mildly increased, by less than twofold, in the soleus (slow-twitch muscle, predominantly oxidative). Furthermore, such muscle-type dependency in fasting-induced transcriptional changes in UCP2, UCP3, carnitine palmitoyltransferase and medium-chain acyl-CoA dehydrogenase persists when the increase in circulating levels of free fatty acids during fasting is abolished by the anti-lipolytic agent nicotinic acid - with blunted responses only in the slow-twitch muscle contrasting with unabated increases in fast-twitch muscles. Independently of muscle type, however, the mRNA levels of peroxisome proliferator-activated receptor gamma are not altered during fasting. Taken together, these studies indicate a close association between fasting-induced changes in UCP2 and UCP3 gene expression with those of key regulators of lipid oxidation, and are hence consistent with the hypothesis that these UCP homologs may be involved in the regulation of lipid metabolism. Furthermore, they suggest that in response to fasting, neither the surge of free fatty acids in the circulation nor induction of the peroxisome proliferator-activated receptor gamma gene may be required for the marked upregulation of genes encoding the UCP homologs and key enzymes regulating lipid oxidation in fast-twitch muscles.

Animals↗
PubMed1988

Mechanism of decreased acetaminophen glucuronidation in the fasted rat.

The mechanism by which an acute fast decreases the glucuronidation of hepatotoxic doses of acetaminophen in the rat was examined. Fasting did not depress the level of the enzyme, glucuronyl transferase, or the basal level of the co-substrate, UDP-glucuronic acid (UDPGA). Administration of a hepatotoxic dose of acetaminophen rapidly depleted UDPGA levels in both fed and fasted rats to the same nadir. Fed and fasted rats differed in that the rate of repletion of UDPGA levels was markedly slower in fasted rats. The total hepatic levels of UDP-glucose dehydrogenase and its cofactor, NAD+, were not decreased by fasting. In fasted rats, hepatic levels of the UDPGA precursor, UDP-glucose, were approximately 60% those of fed rats both before and after a hepatotoxic dose of acetaminophen. In fed rats, acetaminophen induced a marked depletion of hepatic glycogen levels and a dramatic increase in blood glucose levels. Acetaminophen induced a similar marked increase in blood glucose levels in fasted rats in spite of the fact that they lacked hepatic glycogen. It is concluded that the fasting-induced decrease in the glucuronidation of hepatotoxic doses of acetaminophen results from decreased production of UDPGA. The decreased synthetic capacity for UDPGA does not appear to be due to the inability of the liver to produce glucose units per se, but rather to the fasting-induced altered activities of the enzymes of carbohydrate metabolism which, in turn, alter the fate of glucose-6-phosphate derived from gluconeogenesis.

Acetaminophen↗
PubMed1991

Effects of method of preservation on functions of livers from fed and fasted rabbits.

Livers from fed, fasted (48 h) and glucose-fed rabbits were preserved for 24 and 48 h by either simple cold storage (CS) or continuous machine perfusion (MP) with the University of Wisconsin preservation solutions. After preservation liver functions were measured by isolated perfusion of the liver (at 37 degrees C) for 2 h. Fasting caused an 85% reduction in the concentration of glycogen in the liver but no change in ATP or glutathione. Glucose feeding suppressed the loss of glycogen (39% loss). After 24 h preservation by CS livers from fed or fasted animals were similar including bile production (6.2 +/- 0.5 and 5.6 +/- 0.4 ml/2 h, 100 g, respectively), hepatocellular injury (LDH release = 965 +/- 100 and 1049 +/- 284 U/liter), and concentrations of ATP (1.17 +/- 0.15 and 1.18 +/- 0.04 mumol/g, glutathione (1.94 +/- 0.51 and 2.35 +/- 0.26 mumol/g, respectively), and K:Na ratio (6.7 +/- 1.0 and 7.7 +/- 0.5, respectively). After 48 h CS livers from fed animals were superior to livers from fasted animals including significantly more bile production (5.0 +/- 0.9 vs 2.0 +/- 0.3 ml/2 h, 100 g), less LDH release (1123 +/- 98 vs 3701 +/- 562 U/liter), higher concentration of ATP (0.50 +/- 0.16 vs 0.33 +/- 0.07 mumol/g) and glutathione (0.93 +/- 0.14 vs 0.30 +/- 0.13 mumol/g), and a larger K:Na ratio (7.4 vs 1.5). Livers from fed animals were also better preserved than livers from fasted animals when the method was machine perfusion. The decrease in liver functions in livers from fasted animals preserved for 48 h by CS or MP was prevented by feeding glucose. Glucose feeding increased bile formation after 48 h CS preservation from 2.0 +/- 0.3 (fasted) to 6.9 +/- 1.2 ml/2 h, 100 g; LDH release was reduced from 3701 +/- 562 (fasted) to 1450 +/- 154 U/liter; ATP was increased from 0.33 +/- 0.07 (fasted) to 1.63 +/- 0.18 mumol/g; glutathione was increased from 0.30 +/- 0.01 (fasted) to 2.17 +/- 0.30 mumol g; and K:Na ratio was increased from 1.5 +/- 0.9 to 5.3 +/- 1.0. This study shows that the nutritional status of the donor can affect the quality of liver preservation. The improvement in preservation by feeding rabbits only glucose suggests that glycogen is an important metabolite for successful liver preservation. Glycogen may be a source for ATP synthesis during the early period of reperfusion of preserved livers.

Adenosine Triphosphate↗
PubMed1991

Short-term fasting increases biliary calcium and bilirubin.

Fasting has been associated clinically with the development of gallbladder sludge and pigment gallstones, both of which are composed primarily of calcium bilirubinate. Although fasting has been demonstrated to increase the cholesterol saturation of bile, its effect on biliary calcium and bilirubin has not been investigated. We, therefore, tested the hypothesis that short-term fasting would increase gallbladder bile calcium and bilirubin levels. Fifteen prairie dogs were studied. Seven animals were not fasted, whereas eight were fasted for 16 hr prior to acute experiments. Gallbladder and hepatic bile samples were obtained and analyzed for calcium, bilirubin, pH, and biliary lipids. Gallbladder bile ionized calcium levels were significantly increased in fasted animals (1.7 +/- 0.2 mM) compared to those in nonfasted animals (1.1 +/- 0.1 mM). Similarly, total calcium (4.3 +/- 0.5 mM vs 2.3 +/- 0.3 mM), total bilirubin (63 +/- 12 microM vs 29 +/- 8 microM), and bilirubin monoglucuronide (58 +/- 10 microM vs 22 +/- 8 microM) were significantly increased in the fasted group. Fasted animals were also noted to have an increased biliary cholesterol saturation index (0.57 +/- 0.04 vs 0.36 +/- 0.03) and decreased biliary pH (6.9 +/- 0.1 vs 7.6 +/- 0.1). These data indicate that in the prairie dog short-term fasting results in significant alterations in gallbladder bile composition. The increased concentrations of gallbladder calcium and bilirubin observed in these experiments may account, in part, for the formation of pigment gallstones and gallbladder sludge seen clinically with prolonged fasting.

Animals↗
PubMed1996

Ventromedial hypothalamic lesions prevent the fasting-induced changes in day-night pattern of locomotor activity.

The time-course of day-night organization of running wheel activity during prolonged fasting was studied in rats, with or without electrolytic lesions in the ventromedial hypothalamus (VMH). For each individual, dates were referenced to the metabolic transition from lipid to protein utilization in late fasting; this was estimated by daily weighing. In fasted sham-operated controls, daytime activity increased progressively over the fast. This fasting-induced rise in diurnal activity was not due to daily handling, since it was observed also in non-handled (fasted) controls. The pattern of the increase in sham-operated rats differed between 2-hour periods (8-10 h to 18-20 h). The distribution of nocturnal activity was also modified during food deprivation: nocturnal activity in late fasting increased in the 20-22 h period and concomitantly decreased in the two 4-6 h and 6-8 h periods. By contrast, VMH lesions markedly limited and delayed the rise in diurnal running activity, irrespective of the 2-hour period. They prevented any significant change in nocturnal activity pattern over the fast. In fasted sham-operated rats, the data may be interpreted as a phase-advance of the nocturnal pattern of locomotor activity, concomitant with the increase of activity during daytime. These changes were suppressed by the VMH lesions. This suggests that the fasting-induced changes in the day-night pattern of locomotor activity are centrally mediated by a neuronal circuit involving the ventromedial hypothalamus.

Animals↗
PubMed1985

Intestinal brush border membrane marker enzymes, lipid composition and villus morphology: effect of fasting and diabetes mellitus in rats.

Diabetes mellitus is associated with enhanced passive intestinal uptake of cholesterol and fatty acids. In order to determine the basis for these changes in intestinal permeability, the jejunal morphology and the lipid content of purified brush border membranes (BBM) were measured in fasted and fed control (C) and streptozotocin diabetic (DM) rats. There was no difference between C and DM in BBM sucrase or alkaline phosphatase; fasting had no effect on BBM enzymes in C, but in DM fasting was associated with increased sucrase activity per length of jejunum. In C fasting was associated with higher levels of BBM total phospholipid, lecithin, choline and amine phospholipids, whereas fasting in DM was associated with higher BBM cholesterol and lower free fatty acids. In the fasting DM, there was a greater villus and mucosal surface area than in the fasting C. A previous study demonstrated that with fasting in DM versus C, cholesterol uptake was unchanged, but when animals were fed, cholesterol and fatty acid uptake were greater into the jejunum of fed DM as compared with fed C. In the BBM of fed DM as compared with C, there was a significant increase in total phospholipid, lecithin, phosphatidyl ethanolamine, choline and amine phospholipids, and phospholipid/cholesterol ratio. Thus, (1) fasting is associated with changes in intestinal morphology, BBM lipids; (2) the effect of fasting is different in DM and C; (3) the enhanced uptake of lipids into the jejunum of fed diabetic rats is not due to changes in villus morphology, but may be due to alterations in the BBM phospholipids.

Alkaline Phosphatase↗
PubMed2004

Hepatopancreas gluconeogenesis and glycogen content during fasting in crabs previously maintained on a high-protein or carbohydrate-rich diet.

The present study assessed the effect of different fasting times on the in vitro gluconeogenic capacity of Chasmagnathus granulata crabs previously adapted to a high-protein (HP) or carbohydrate-rich (HC) diet using the incorporation of [U-(14)C]l-lactate or [U-(14)C]l-alanine into glucose. We also recorded haemolymphatic glucose and hepatopancreatic glycogen levels. In the HP group, on the third day of fasting there were decreases in the synthesis of glucose from (14)C-alanine and in haemolymph glucose. After 15 days of fasting, haemolymph glucose and hepatopancreatic glycogen levels were maintained by an increase in the conversion of (14)C-alanine into glucose. However, after 21 days of fasting the gluconeogenic capacity was decreased and hepatopancreas glycogen concentration was reduced. In the HC group, hepatopancreatic glycogen was the energy source during the first 6 days of fasting. Gluconeogenesis from (14)C-lactate decreased after 6 days of fasting, remaining low until 21 days of fasting. The conversion of (14)C-alanine into glucose was increased after 15 days fasting and hepatopancreatic glycogen was raised in relation to that present after a 6-day fasting. In both dietary groups the stabilization in the levels of haemolymph glucose after 21 days fasting may result from a reduction in metabolic rate during restricted feeding.

Alanine↗
PubMed2005

Effects of short-term fasting on energy reserves of vampire bats (Desmodus rotundus).

Studies on metabolic responses to fasting in common vampire bats (Desmodus rotundus) have demonstrated the susceptibility of this species when subjected to long-term fasting. We investigated the effects of short-term fasting (12 h), a period similar to what they face in the field, on their energy reserves. Blood glucose (BG) levels in fed bats were similar to other mammals, but after 12 h without food, these levels were reduced. Plasma lactate and free fatty acids levels in fed bats were higher than in other mammals, although no changes in these levels were detected in response to fasting. Liver glycogen content decreased significantly following fasting. Muscle glycogen, as well as liver and muscle lipid and protein levels, remained unaltered for up to 12 h of fasting. Although BG levels decreased after short-term fasting, body energy reserves do not seem to play an important role for maintenance of glycemic homeostasis during fasting. Despite the decrease in liver glycogen, this small reserve seems insufficient to maintain adequate levels of BG, even during short periods of fasting. Because other reserves were not decreased after fasting, it is possible that the main source of glucose for common vampire bats might be the glucose content of their blood diet.

Animals↗
PubMed1999

Regulation of glycogen utilization in ischemic hearts after 24 hours of fasting.

INTRODUCTION: Fasting protects the ischemic heart from injury and infarction. Previous studies have shown that hearts from fasted animals have greater glycogen utilization and a lower cytosolic redox state (NADH/NAD+) during global ischemia. While the mechanisms of increased glycogen utilization in fasted animals have not been elucidated, animals that hibernate or are tolerant of anoxia are known to increase the tissue content of the active form of glycogen phosphorylase, phosphorylase a. Therefore, this study was designed to (a) determine whether hearts from fasted animals have increased activity of glycogen phosphorylase during ischemia and (b) define those mechanisms responsible for this increase. METHODS: Hearts isolated from either fed or fasted (24 h) rats were perfused and freeze-clamped at baseline, and after 1 and 10 min of ischemia, for measurement of phosphorylase activity, phosphorylase kinase activity, and glucose-6-phosphate concentrations. RESULTS: Fasting increased the phosphorylase a/b ratio under both baseline and ischemic conditions. This increase was not accompanied by an increase in the activity of phosphorylase kinase, either with maximal [Ca2+] or under physiologic [Ca2+]. Glucose 6-phosphate concentrations were lower in hearts from fasted animals under baseline, but not ischemic, conditions. CONCLUSIONS: Fasting enhances glycogen utilization during ischemia by increasing the active form of glycogen phosphorylase. This increase is not due to a change in phosphorylation by phosphorylase kinase nor end-product inhibition by G-6P. While the precise mechanism of increased glycogen phosphorylase activity in fasted animals is not clear, one likely explanation may be the lower cytosolic redox state demonstrated in the myocardium of fasted animals.

Analysis of Variance↗
PubMed1997

Fasting-induced suppression of hypothalamic-pituitary-gonadal axis in the adult rhesus monkey: evidence for involvement of excitatory amino acid neurotransmitters.

The present study was designed to examine whether acute food-restriction in non-human primates, suppresses hypothalamic-pituitary-testicular (HPT) axis via alterations in the excitatory amino acid (EAA) neurotransmitter-utilizing drive to the GnRH neuron. This was achieved indirectly by comparing the plasma testosterone (T) responses to administration of an excitatory amino acid analogue, N-methyl-D,L-aspartic acid (NMA), in acutely fasted and normal fed monkeys. A set of 4 chair-restrained adult male rhesus monkeys, was assigned to the following treatments: a) normal feeding, b) one-day fasting (omission of morning and afternoon meals), c) normal feeding+NMA (15 mg/kg BW) and d) one-day fasting+NMA (15 mg/kg BW). Starting 1 h after the provision or omission of the afternoon meal, frequent blood sampling was initiated at 15-min intervals for a period of 3-h. NMA was administered as an iv bolus 1 h after start of the sampling. Secretion of T was affected (P<0.005) by the treatments. A peak in T was evident during the first h of the sampling in fed but not fasted monkeys. Mean 3-h T concentrations were suppressed (P<0.001) by the fasting. Administration of NMA in fasting conditions resulted into an acute stimulation of T secretion in 2 of the 4 monkeys. However, mean 60-min post-NMA T concentrations were greater (P<0.05) than those prevailing during the same period in fasted animals not given NMA. In contrast, all 4 fed-monkeys showed significant T elevations in plasma immediately following the NMA challenge and mean T levels during the 60-min post-NMA period were higher (P<0.05) than those in fed animals not injected with NMA, at a comparable time. Testosterone area under the curve for the 2-h post-NMA period was greater (P<0.05) in fed- than in fasted-monkeys. These results indicate that although NMA can stimulate GnRH release both in fed and short-term fasting conditions, the response appears to be suppressed in the later situation suggesting that fasting-induced suppression of the HPT axis in the adult male rhesus monkey may involve a reduction in the sensitivity of GnRH neurons to the EAA neurotransmission.

Animals↗
PubMed2003

The relationship between nonfasting and fasting lipid measurements in patients with or without type 2 diabetes mellitus receiving treatment with 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors.

BACKGROUND: Studies have confirmed a lack of patient and physician adherence to the revised National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) guidelines. These guidelines state that lipid panels should be obtained while the patient is in the fasting state. However, this restriction may limit the ordering of these tests and thus decrease the number of patients on drug therapy and the number treated until goal cholesterol levels are reached. Evidence shows that testing in the nonfasting state may not be clinically or significantly different from testing in the fasting state in identifying patients at risk for a future cardiovascular event. OBJECTIVES: The purpose of this study was to determine whether a relationship exists between nonfasting and fasting lipid values in diabetic or nondiabetic patients that will permit the more ready identification of patients who require treatment to meet NCEP ATP III guidelines. A secondary goal was to determine whether diabetic patients who appear to have reached goal cholesterol levels in the fasting state meet those goals when the non-high-density lipoprotein cholesterol (HDL-C) levels are measured in the nonfasting state. METHODS: This observational study was conducted at Androscoggin Cardiology Associates (Auburn, Maine). Patients with hyperlipidemia receiving statin therapy whose doses had not changed for > or =2 months were enrolled. For all patients, nonfasting and fasting lipid panels (total cholesterol, triglycerides [TGs], and HDL-C) were calculated, whereas low-density lipoprotein cholesterol (LDL-C)levels were measured directly. The direct LDL-C method was used to determine the variance of the calculated LDL-C from the actual value. RESULTS: One hundred consecutive hyperlipidemic patients were tested. Patients included 70 men and 30 women, with a mean (SD) age of 66.2 (12.0) years(range, 24-93 years). Eighteen patients had type 2 diabetes mellitus (DM). Non-fasting TG, HDL-C, and LDL-C levels were able to identify almost all patients who did not meet ATP III guidelines in terms of cholesterol levels (95%, 100%, and 95%, respectively). No predictive differences were found, regardless of whether the patients had type 2 DM. For the total population, statistically significant differences were found between calculated nonfasting and fasting measurements for mean (SD)LDL-C levels (90.2 [24.8] mg/dL vs 99.7 [26.1] mg/dL, respectively; P < 0.001). The regression equation was fasting LDL-C = 22.7 + 0.854 x nonfasting LDL-C.A nonfasting LDL-C level >130 mg/dL predicted a fasting LDL-C level >100 mg/dL(95% CI, -12.79 to -6.24), and a nonfasting LDL-C level >130 mg/dL predicted cases of fasting LDL-C level >100 mg/dL (95% CI, -5.79 to -1.35). CONCLUSIONS: In this study population, nonfasting TG, HDL-C, and LDL-C levels successfully identified almost all patients who did not meet ATP III guidelines for cholesterol levels. No clinically significant difference was found in diabetic or nondiabetic patients.

Adult↗
PubMed2002

Body burdens and tissue concentrations of organochlorines in polar bears (Ursus maritimus) vary during seasonal fasts.

Lipophilic organochlorines (OCs) are ingested by mammals through their foods and are generally stored in adipose tissue depots. For some species, such as polar bears, the size of these depots can fluctuate seasonally by several-fold. However, the effect of these fluctuations on the fate of stored OCs in an animal with such labile lipid depots is unknown. We determined the whole body burden and tissue concentrations of OCs in free-ranging polar bears categorized by age (cubs-of-the-year, yearlings and adults) and sex before and after a fast averaging 56 days. Adipose tissue, plasma, and milk samples were analysed for sum of chlorobenzenes (sigma-ClBzs), hexachlorocyclohexanes (sigma-HCHs), chlordanes (sigma-CHLORs), dichlorodiphenyltrichloroethane compounds (sigma-DDTs) and polychlorinated biphenyls (sigma-PCBs). Decline in body mass during fasting ranged from 0.2 kg/day for cubs-of-the-year to 0.9 kg/day for sub-adult and adult males. Although all bears showed a decline in both lipid and lean mass during fasting, patterns of OC whole body burden changes were not consistent among compounds and bear classes. The burdens of sigma-DDTs declined by 11-50% for most bears during fasting, those of sigma-CHLORs declined by 67% during fasting in sub-adult and adult males but remained constant for all females, indicating male-specific metabolism of sigma-CHLORs. As fat depots became depleted, OC concentrations in the remaining adipose tissue varied; sigma-DDTs and sigma-HCHs declined while those of sigma-CHLORs and sigma-PCBs generally increased. Thus. within a 3-4 month fast, most polar bears were able to significantly rid their adipose tissue of sigma-DDTs and sigma-HCHs. Burdens of sigma-CHLORs (except males), sigma-ClBzs and sigma-PCBs remained constant for all classes of bears, therefore there was no significant excretion or metabolism during the fast of the specific congeners in these compound classes typically found in polar bears. The ratio of plasma/adipose tissue and milk/adipose tissue OC concentrations was the same for before and after the fast indicating that OC concentrations in polar bears are probably at a steady state among various body compartments. Concentrations of sigma-CHLORs and sigma-PCBs in milk almost doubled during the fast. As a consequence of this rise in milk OC concentrations, the whole body concentrations of these compounds increased in nursing cubs. Since developing young may be susceptible to the effects of environmental contaminants, the increased exposure of nursing cubs to OCs during a fast by their mothers is noteworthy.

Adipose Tissue↗
PubMed1980

Renal brush border membrane adaptation to phosphorus deprivation: effects of fasting versus low-phosphorus diet.

Alimentary phosphorus deprivation due to a low-phosphorus diet (LPD) elicits a profound antiphosphaturia and an increase in sodium-dependent inorganic phosphate (Pi) uptake by renal cortical brush border membrane (BBM) vesicles. But, in alimentary phosphorus deprivation due to total fasting, high urinary excretion of Pi persists. In the present study, we determined whether low tubular reabsorption of Pi in fasting is due to a diminished capacity of the specific Pi transport system with the renal cortical luminal BBM or whether it is due to a reduced transepithelial reabsorption of Pi because of metabolic conditions occurring in proximal tubule cells during fasting. Sodium-dependent Pi transport in compared with fasted rats or rats fed a normal phosphorus diet. Sodium-dependent uptake of D-glucose was significantly lower in LPD rats, compared with fast animals or animals fed a normal diet. Thus, in contrast to LPD, fasting does nt elicit an increase in Pi transport and a decrease in D-glucose transport across the isolated renal BBM. The same differences in BBM transport of Pi were present also in thyroparathyroidectomized rats. Further experiments demonstrated that the adaptation of renal function and the renal BBM transport to LPD are overridden by a subsequent period of total fasting. Results of the present study show that fasting both prevents and reverses the renal response of rats to alimentary phosphorus deprivation. The differences in Pi excretion between fasted rats, LPD rats, and LPD rats subsequently fasted are attributed, at least in part, to specific adaptive changes in sodium-dependent Pi transport across the luminal BBM, rather than to alterations in other cellular (metabolic) components of transepithelial Pi reabsorption in the proximal tubule.

Animals↗
PubMed2004

Association between indices of obesity and fasting hyperglycemia in Taiwan.

OBJECTIVE: To examine the association of body mass index (BMI), waist-hip ratio (WHR), and waist circumference (WC) with fasting hyperglycemia after adjustment for age, cigarette smoking, and alcohol use. DESIGN: A cross-sectional survey was conducted among individuals visiting four health-screening centers across Taiwan. SUBJECTS: A total of 61 568 subjects (28 734 men and 32 834 women) between 25 and 64 years of age were included. Fasting hyperglycemia was defined as fasting plasma glucose > or =6.1 mmol/l or current diagnosis and use of insulin or hypoglycemic agent. RESULTS: Fasting hyperglycemia was found in 11.0% of men and 8.3% of women. The factors significantly associated with fasting hyperglycemia in men were age, BMI, WHR, and heavy drinking, while for women these factors were age, educational level, BMI, WHR, and heavy smoking. For men, increased risk of fasting hyperglycemia started from age 30 to 34 years, BMI > or =25 kg/m2, and WHR > or =0.82. For women, increased risk of fasting hyperglycemia started from age 35 to 39 years, BMI > or =24 kg/m2, and WHR > or =0.74. WC lost its significance as a predictor of fasting hyperglycemia when WHR included in the model. CONCLUSION: This study found that central obesity and general obesity were both independently associated with increased risk of fasting hyperglycemia in Taiwanese. The relationship between fasting hyperglycemia and central fat accumulation (WHR) begins to appear at levels that would not be regarded as representing obesity in Western populations, suggesting the need to redefine cutoffs for central obesity in this population.

Adult↗
PubMed1999

The study of spontaneous GH secretion after 36-h fasting distinguishes between GH-deficient and normal adults.

OBJECTIVE: Within an appropriate clinical context, GH deficiency (GHD) in adults can only be diagnosed biochemically by provocative testing. The evaluation of IGF-I, IGFBP-3 and even of spontaneous GH secretion do not establish the diagnosis of adult GHD. In fact, remarkable overlaps between normal and GHD adults have been reported for all these parameters. On the other hand, it is well known that even short-term fasting stimulates GH secretion in normal subjects. The aim of our study was to determine the effects of 36 h fasting on 8-h diurnal GH, insulin and glucose levels as well as on basal IGF-I, IGFBP-3, acid-labile subunit (ALS), IGFBP-1, GHBP and free fatty acid (FFA) levels. SUBJECTS: We studied 9 GHD adults (GHD, 8 males, 1 female; age, mean +/- SEM: 37.6 +/- 2.3 years, body mass index (BMI): 24.5 +/- 1.0 kg/m2) and 20 age-matched normal subjects (NS) as controls (13 males, 7 females; age: 28.9 +/- 0.6 years, BMI: 21.6 +/- 0.4 kg/m2). STUDY DESIGN: In all subjects we studied the effects of 36 h fasting on 8-h daytime GH, insulin and glucose levels (assay every 30 min from 0800 h to 1600 h) as well as on basal IGF-I, IGFBP-3, ALS, IGFBP-1, GHBP and FFA levels. RESULTS: Before fasting, basal mean IGF-I, IGFBP-3 and ALS levels in GHD were lower (P < 0. 0001) than in NS. IGFBP-1, GHBP and FFA levels were similar in both groups. Before fasting mean GH concentration (mGHc) in GHD was lower (P < 0.05) than in NS (0.4 +/- 0.2 vs. 2.2 +/- 0.6 mu/l) but with a clear overlap between the 2 groups (range 0.4-0.8 vs. 0.4-6.8 mu/l). After fasting, both in GHD and NS basal IGF-I, IGFBP-3, ALS and GHBP levels did not change significantly. On the other hand, in both GHD and in NS IGFBP-1 was increased (P < 0.0001) to a similar extent, while FFA increased in NS more (P < 0.01) than in GHD. Fasting significantly increased mGHc in NS (12.0 +/- 1.2 mu/l, P < 0.0001) but not in GHD (0.6 +/- 0.2 mu/l). After fasting, no overlap was present between GHD and NS (0.4-1.6 vs. 2.4-20.8 mu/l, respectively). Mean glucose and insulin concentrations over 8 h in GHD and NS in basal conditions were similar and were reduced to the same extent in both groups. CONCLUSIONS: Our findings demonstrate that after short-term fasting, the study of spontaneous GH secretion distinguishes between GH-deficient adults and normal subjects; this phenomenon occurs before significant changes in IGF-I and IGFBP-3 levels. These results suggest that the assessment of spontaneous GH secretion could be useful for the diagnosis of adult GH deficiency only after short-term fasting.

Adult↗
PubMed2003

Fasting insulin sensitivity and post-oral glucose hyperinsulinaemia related to cardiovascular risk factors in adolescents with precocious pubarche.

OBJECTIVE: Adolescents and young women with a history of precocious pubarche (PP, appearance of pubic hair before 8 years) exhibit hyperlipidaemia, and ovarian hyperandrogenism, indicating increased risk of coronary heart disease in the long term. The aim of this study was to determine the relative contribution of fasting insulin sensitivity, and post oral glucose tolerance test (OGTT) measures of insulin secretion to metabolic risk markers of adult disease. PATIENTS AND DESIGN: We have analysed data from 51 young women presenting with isolated PP (age range, 5.9-19.0 years) in early, mid and late puberty and 68 puberty-matched controls (age range, 6.2-16.8 years). Body composition data from a further 67 girls with PP are also presented. MEASUREMENTS: The homeostasis model of assessment insulin sensitivity index (HOMA Si) based on fasting glucose and insulin measurements and MSI120 based on insulin levels over the first 120 min following standard oral glucose load were selected as measures of fasting insulin sensitivity and 0-120-min insulinaemia, respectively. ISI30 was used as an index of insulin secretion 30 min following oral glucose load. RESULTS: The physiological decrease in fasting insulin sensitivity, 30-min insulin secretion and 0-120-min insulinaemia during puberty were exaggerated in PP girls. The relationship between fasting insulin sensitivity and 0-120-min insulinaemia was similar in PP girls and in controls but at each level of fasting insulin sensitivity the PP girls had a higher level of insulin secretion in response to an oral glucose load (P < 0.001). Fasting insulin sensitivity and 0-120 minute insulinaemia but not 30-min insulin secretion were strongly related to known cardiovascular risk factors. In a multivariate model incorporating fasting insulin sensitivity, 0-120-min insulinaemia, pubertal stage and body mass index (BMI) SDS as covariates, 0-120-min insulinaemia was strongly associated with elevated free androgen index, total cholesterol and truncal fat mass (P < 0.001) whereas fasting insulin sensitivity was associated only with reduced free androgen index (P < 0.02). CONCLUSIONS: Chronic exposure to insulin as reflected by 0-120 min hyperinsulinaemia, rather than 30 min insulin secretion, or fasting insulin senstivity, was most closely related cardiovascular disease risk in girls with PP.

Adolescent↗
PubMed1999

Post-prandial chylomicron response may be predicted by a single measurement of plasma apolipoprotein B48 in the fasting state.

BACKGROUND: The clearance of chylomicron remnants was assessed in normolipaemic, dyslipidaemic and obese male subjects by monitoring the plasma kinetics of apolipoprotein (apo) B48, retinyl palmitate and triglyceride after a lipid meal. Regression analysis of fasting plasma apo B48 with the area under the post-prandial curves of apo B48, retinyl ester and triglyceride was carried out in order to determine whether the post-prandial response could be predicted by the fasting concentration of this exclusive chylomicron marker. MATERIALS AND METHODS: Fasted subjects were given an oral fat load supplemented with retinyl palmitate, and blood samples were drawn over a 10-h period. Apolipoprotein B48 was determined by Western blotting in the plasma density fraction less than 1.063 g mL-1. Plasma retinyl palmitate and triglyceride were determined by high-performance liquid chromatography (HPLC) and colorimetric procedures respectively. The areas under the apo B48, retinyl ester and triglyceride curves were determined by integration. Relationships between the post-prandial response and the fasting concentration of apolipoprotein B48 were assessed using least-squares regression analysis. RESULTS: We found a strong positive relationship between the fasting plasma concentration of apo B48 and the post-prandial kinetics of apo B48. Similarly, there was a positive relationship of fasting apo B48 with the retinyl ester area under the curve. Collectively, the data suggested that chylomicron remnant kinetics can be predicted based on the fasting level of apo B48. There was also a significant but weaker relationship of fasting apo B48 with post-prandial triglyceride kinetics, consistent with removal of this lipid by hydrolytic mechanisms in addition to particle uptake. CONCLUSION: The fasting plasma concentration of apo B48 appeared to be a good surrogate marker for the degree of post-prandial lipidaemia and may circumvent the need for oral fat challenges. Moreover, in the fasting state apo B48 concentration is a marker of chylomicron remnants, which are considered to be the proatherogenic form of these intestinally derived lipoproteins.

Adolescent↗