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PubMed2005

Leptin concentrations in plasma and follicular fluid from prepubertal gilts as influenced by fasting, refeeding and insulin.

This study's aim was to examine whether fasting and refeeding would influence leptin levels in both plasma and follicular fluid from prepubertal gilts, and whether insulin affects leptin levels in fasting gilts. In experiment 1, four gilts were fasted for 72 h and then refed. Blood samples were withdrawn during normoalimentation, at the end of fasting, and for 4 h after refeeding. All samples were assayed for leptin; alternate samples were assayed for insulin, glucose and non-esterified fatty acids (NEFA). Fasting caused a decrease in leptin, glucose and insulin levels in plasma, while NEFA concentrations increased. In experiment 2, four gilts were given insulin as a bolus (0.2 IU/kg body weight) after 68 h of fasting. Blood samples were collected every 15 min around insulin administration and were assayed for leptin, insulin and glucose. This experiment shows that insulin administration increases leptin levels during fasting. In experiment 3, gilts were ovariectomized during normal alimentation (n=4), after 48 h of fasting (n=4), and after 48 h of realimentation following 48 h of fasting (n=4). Leptin levels in both plasma and follicular fluid collected after 48 h of fasting were significantly lower than those observed during normoalimentation or refeeding. In conclusion, a transient increase in insulin during fasting is effective in restoring leptin concentrations; in addition, leptin levels in follicular fluid parallel those in plasma.

Age Factors↗
PubMed1987

The effect of fasting on enzyme levels in the enlarged and involuting rat pancreas.

1. The effect on pancreatic digestive enzyme levels of fasting and changes from a diet containing trypsin inhibitor (raw soya-bean flour, RSF) to diets free of trypsin inhibitor (heated soya-bean flour, HSF, or commercial rat chow) was studied in rats for up to 7 d. 2. In RSF-fed rats killed without fasting, enzyme levels were low, but after fasting for 24 h before killing there was a marked increase in all enzyme levels. Histological studies showed that pancreatic acinar cells from RSF-fed rats killed without fasting were devoid of zymogen granules, but following a 24 h fast there was a marked accumulation of zymogen granules which extend into the basal cytoplasm. Fasting either produced no change or a fall in enzyme levels in rats fasted after feeding HSF or chow continuously. 3. If animals fed on RSF were changed to HSF and either fed or fasted for 24 h up to the time of killing there was an increase in amylase (EC 3.2.1.1), trypsin (EC 3.4.21.4), lipase (triacylglycerol lipase; EC 3.1.1.3) and protein 1 d after the change, followed by a fall over the next 6 d to levels similar to those seen in rats fed on HSF continuously. 4. Animals changed from RSF to chow showed similar effects as far as trypsin, lipase and protein were concerned, but amylase rose, to reach the level seen in rats fed on chow continuously (about ten times that seen in soya-bean-fed rats), after 2 d. 5. These results suggest that in the rats fed on RSF, pancreatic enzyme synthesis is rapid but secretion is equally rapid and intracellular enzyme levels are low. When these animals are fasted or changed to a diet free of trypsin inhibitor the rate of secretion falls but the high rate of synthesis continues for at least 24 h and enzymes accumulate in the pancreas. In studies of pancreatic enzyme levels in rats fed on trypsin inhibitor the extent of fasting before killing the animal is therefore an important variable. Such animals should probably not be fasted before study.

Animals↗
PubMed1993

Livers from fasted rats acquire resistance to warm and cold ischemia injury.

Successful liver transplantation is dependent upon many factors, one of which is the quality of the donor organ. Previous studies have suggested that the donor nutritional status may affect the outcome of liver transplantation and starvation, due to prolonged stay in the intensive care unit, may adversely affect the liver. In this study we have used the orthotopic rat liver transplant model to measure how fasting the donor affects the outcome of liver transplantation. Rat livers were preserved with UW solution either at 37 degrees C (warm ischemia for 45-60 min) or at 4 degrees C (cold ischemia for 30 or 44 hr). After preservation the livers were orthotopically transplanted and survival (for 7 days) was measured, as well as liver functions 6 hr after transplantation. After 45 min of warm ischemia 50% (3 of 6) animals survived when the liver was obtained from a fed donor about 80% (4 of 5) survived when the liver was obtained from a three-day-fasted donor. After 60 min warm ischemia no animal survived (0 of 8, fed group). However, if the donor was fasted for 3 days 89% (8 of 9) of the animals survived for 7 days. Livers cold-stored for 30 hr were 50% viable (3 of 6) and fasting for 1-3 days did not affect this outcome. However, if the donor was fasted for 4 days 100% (9 of 9) survival was obtained. After 44-hr preservation only 29% (2/7) of the recipients survived for 7 days. If the donor was fasted for 4 days, survival increased to 83% (5/6). Liver functions, bile production, and serum enzymes were better in livers from the fasted rats than from the fed rats. Fasting caused a 95% decrease in liver glycogen content. Even with this low concentration of glycogen, liver viability (animal survival) after warm or cold ischemia was not affected, and livers with a low glycogen content were fully viable. Thus liver glycogen does not appear to be important in liver preservation. This study shows that fasting the donor does not cause injury to the liver after warm or cold ischemia. In fact, the livers appeared to be better able to tolerate ischemia when obtained from fasted rats. Thus donor nutritional status may be an important factor for outcome of liver transplantation. Livers from fasted donors may be capable of tolerating long-term preservation better than livers from fed donors.

Adenosine↗
PubMed2004

Leptin-mediated effects of undernutrition or fasting on luteinizing hormone and growth hormone secretion in ovariectomized ewes depend on the duration of metabolic perturbation.

We aimed to determine the importance of leptin in the regulation of luteinizing hormone (LH) and growth hormone (GH) secretion in ovariectomized (OVX) ewes. Lean and fat sheep were produced by dietary manipulation over 8 months and were then fasted for 32 h. Plasma concentrations of glucose, insulin and leptin were higher in the fat group. Fasting decreased plasma concentrations of glucose and insulin and increased concentrations of nonesterified fatty acids (NEFA) in fat and lean ewes, but leptin concentrations were reduced in the fat group only. Plasma GH concentrations were higher in the lean group and LH concentrations were lower; there was no effect of fasting. These data suggested that long-term changes in plasma leptin concentrations might affect LH and GH secretion, but acute changes with fasting had no effect. OVX ewes of normal body weight were fasted for 72 h with or without intracerebroventricular (i.c.v.) infusion of leptin (4 microg/h), achieving similar metabolic effects to the 32 h fast. The 72-h fast increased LH pulse amplitude, mean GH and cortisol concentrations, but these changes were corrected towards normal by leptin treatment. Thus, leptin could attenuate fasting-induced alterations in the secretion of LH, GH and cortisol. Finally, we food-restricted OVX ewes for 4 months (lean), leading to a 20-kg reduction in body weight. Plasma concentrations of leptin and insulin were decreased, and plasma GH concentrations increased, but there was no effect on plasma concentrations of LH, glucose or NEFA. Icv infusion of leptin did not affect any endocrine or metabolic parameter in these ewes. In summary, maintenance of a lean or fat condition for a prolonged period (8 months) or an extended fasting (72 h) can affect LH and GH secretion, but short-term food restriction (4 months) affected only GH secretion and short-term fasting (32 h) had no effect on either LH or GH secretion. This is in spite of altered plasma leptin concentrations in all circumstances studied. Although leptin treatment can restore plasma concentrations of LH, GH and cortisol towards normal in sheep fasted for 72 h, some other factor(s) must signal to the brain to cause shifts in neuroendocrine function in other conditions where nutritional/metabolic status is altered.

Animals↗
PubMedDate not supplied

Effect of fasting on the activity and turnover of rat liver alcohol dehydrogenase.

Alcohol dehydrogenase activity in rat liver decreased with fasting to about 60% of the fed level, but the specific activities of the enzyme purified from livers of fed and 12- or 48-hr fasted animals were similar, 3.2-3.4 U/mg protein. Therefore, the decrease in enzyme activity with fasting should have resulted from a decrease in the amount of enzyme protein. Accordingly, the turnover of alcohol dehydrogenase was examined in fed and fasted rats. The fractional rate of enzyme synthesis (ks) in fed rats was determined by radioisotopic methods to be 0.13 day-1 and it increased to 0.18 day-1 after a 12- or 48-hr fast. The absolute rate of synthesis (V) and the fractional rate of degradation (kd) were calculated from these ks values and the total enzyme content in livers from animals that were fasted for 8 to 72 hr. After 48-72 hr of fasting, V decreased 16% and kd increased about 20% with respect to the fed values. Together, these changes accounted for the lowered enzyme activity in the fasted state. The rapid decrease in enzyme activity with fasting, t1/2 congruent to 16 hr, was found to be due to a rapid increase in kd from 0.14-0.16 day-1 in fed animals to 0.61 day-1 during the first 8 hr after the initiation of fast. Thereafter, kd decreased steadily to reach 0.18 day-1 after 48-72 hr of fasting.

Alcohol Dehydrogenase↗
PubMed1980

Effects of fasting on the diuretic response and disposition of furosemide in rats.

The influence of fasting on the relationship between the disposition and diuretic effect of furosemide was studied in rats. Fasting consisted of withholding solid food, but not water, for a period of 16 h before administering furosemide (10 mg/kg, sc) or a saline vehicle. Normally fed animals also received furosemide or the vehicle. Fasting did not modify the diuretic or the natriuretic effect (per 100 g body weight) of furosemide. The distribution of total furosemide in plasma or tissues was not affected by fasting. On the other hand, fasting which produced increasing amounts of endogenous free fatty acids in plasma and kidneys increased the concentration of free furosemide in fasting plasma but not in fasting kidney or liver of rats. The in vitro binding constant of furosemide to physiological concentrations of plasma proteins was decreased from the control value by a factor of 6.5 as a result of fasting. Neither unchanged furosemide nor its metabolite in the urine was affected by fasting. Incubation of kidney cortex tissue slices with furosemide both in the presence and absence of free fatty acid indicated an inhibition of furosemide uptake in a manner closely parallel to inhibition by probenecid. Thus, failure to observe a more pronounced diuretic and saluretic effects of furosemide in fasted rats, in spite of higher concentration of free plasma furosemide, might be due to the inhibitory effect of endogenous free fatty acids and (or) other endogenous substances on the uptake of furosemide by renal tubular cells although some homeostatic control mechanisms related to fasting could also be involved.

Animals↗
PubMed1990

Importance of blood glucose concentration in regulating lipolysis during fasting in humans.

The importance of the decline in blood glucose concentration on lipolysis and the lipolytic effect of epinephrine was evaluated during short-term fasting. Lipolytic rates were determined by infusing [2H5]glycerol and [1-13C]palmitic acid. Five volunteers were studied after 12 h of fasting before and during epinephrine infusion and after 84 h of fasting, before and during glucose infusion when plasma glucose was restored to postabsorptive values, and during glucose plus epinephrine infusion. In another protocol, five volunteers were given glucose intravenously throughout fasting to maintain plasma glucose at postabsorptive levels and isotopic studies were performed after 12 and 84 h of fasting before and during epinephrine infusion. Glucose infusion after 84 h of fasting restored glucose and insulin concentrations and lipolytic rates toward 12-h fasting values. When euglycemia was maintained throughout fasting, plasma insulin still declined (P less than 0.05) and lipolytic rates still increased (P less than 0.05). Despite similar glucose concentrations, the lipolytic response to epinephrine infusion was greater after 84 h than after 12 h of fasting in both protocols (P less than 0.05). These studies demonstrate that the decline in plasma glucose contributes to, but is not required for, the increase in lipolysis during fasting. The increase in epinephrine-stimulated lipolysis that occurs during fasting is not dependent on a decrease in plasma glucose concentration.

Adult↗
PubMed1986

Metabolic responses to exercise after fasting.

Fasting before exercise increases fat utilization and lowers the rate of muscle glycogen depletion. Since a 24-h fast also depletes liver glycogen, we were interested in blood glucose homeostasis during exercise after fasting. An experiment was conducted with human subjects to determine the effect of fasting on blood metabolite concentrations during exercise. Nine male subjects ran (70% maximum O2 consumption) two counterbalanced trials, once fed and once after a 23-h fast. Plasma glucose was elevated by exercise in the fasted trial but there was no difference between fed and fasted during exercise. Lactate was significantly higher (P less than 0.05) in fasted than fed throughout the exercise bout. Fat mobilization and utilization appeared to be greater in the fasted trial as evidenced by higher plasma concentrations of free fatty acids, glycerol, and beta-hydroxybutyrate as well as lower respiratory exchange ratio in the fasted trial during the first 30 min of exercise. These results demonstrate that in humans blood glucose concentration is maintained at normal levels during exercise after fasting despite the depletion of liver glycogen. Homeostasis is probably maintained as a result of increased gluconeogenesis and decreased utilization of glucose in the muscle as a result of lowered pyruvate dehydrogenase activity.

3-Hydroxybutyric Acid↗
PubMed2005

Expression analysis of hypothalamic and pituitary components of the growth hormone axis in fasted and streptozotocin-treated neuropeptide Y (NPY)-intact (NPY+/+) and NPY-knockout (NPY-/-) mice.

In the fasted and the streptozotocin (STZ)-induced diabetic male rat, hypothalamic growth hormone (GH)-releasing hormone (GHRH) mRNA levels, and pulsatile GH release are decreased. These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY(+/+)) and NPY-knockout (NPY(-/-)) mice by ribonuclease protection assay. In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. Under fed conditions the GH axis of NPY(+/+) and NPY(-/-) did not differ. In the NPY(+/+) mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. In the NPY(-/-) mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. Fasting resulted in an overall increase in circulating GH, which reached significance in the fasted NPY(-/-) mouse. Induction of diabetes in NPY(+/+) mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. Induction of diabetes in NPY(+/+) and NPY(-/-) mice, using a multiple, low-dose, STZ paradigm (5 consecutive daily injections of 40 mg/kg), did not alter body weight, hypothalamic neuropeptide expression or pituitary receptor expression, with the exception that sst2 mRNA levels were suppressed and GH levels did rise in the NPY(-/-) mouse. These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. In contrast to the rat, fasting clearly did not suppress circulating GH levels in mice, but resulted in an overall rise in mean GH levels, similar to that observed in other mammalian species. The fact that many of the fasting-induced changes in the GH axis were observed in the high-dose STZ-treated mice, but were not observed in the multiple, low-dose paradigm, suggests STZ-mediated modulation of GH axis function is dependent on the severity of the catabolic state and not hyperglycemia.

Animals↗
PubMed2000

Low fasting plasma glucose level as a predictor of cardiovascular disease and all-cause mortality.

BACKGROUND: Although medical textbooks usually classify fasting plasma glucose <70 or 80 mg/dL (<3.89 or 4.44 mmol/L) as abnormal, the prognosis for patients with low fasting plasma glucose is unclear. METHODS AND RESULTS: We conducted prospective cohort studies among 40 069 men and women to investigate the association between fasting plasma glucose levels and cardiovascular disease and all-cause mortality. We documented a U-shaped relation between fasting plasma glucose and mortality. In addition to diabetes and impaired fasting glucose levels, low fasting plasma glucose levels were also associated with high mortality. After multivariate adjustment for age, sex, study population, ethnicity, current smoking status, high blood pressure, total cholesterol, body mass index, triglycerides, history of cardiovascular disease and cancer, and a family history of cardiovascular disease, patients with fasting plasma glucose <70 mg/dL (<3.89 mmol/L) had a 3.3-fold increased risk of cardiovascular disease mortality, and patients with fasting plasma glucose 70 to 79 mg/dL (3.89 to 4.43 mmol/L) had a 2.4-fold increased risk compared with the risk in patients with fasting plasma glucose 80 to 109 mg/dL (4.44 to 6.05 mmol/L) (tests for trend P<0.0001). Participants with low fasting plasma glucose levels also had increased risk of all-cause mortality (test for trend P<0.0001). CONCLUSIONS: Participants with low fasting plasma glucose levels had a high risk of cardiovascular disease and all-cause mortality.

Adult↗
PubMed1988

The effect of fasting on rat portal venous and aortic blood glucose, lactate, alanine, and glutamine.

Using a chronically catheterized rat model, the effect of fasting on portal venous, aortic, and venous blood concentration minus aortic blood concentration ([PV-A]) blood glucose, lactate, alanine, and glutamine concentrations was determined. It has been postulated that the intestine is a source of lactate and alanine, precursors for glycogen synthesis, in the fed state. After 48 h of fasting portal venous glucose, lactate, and alanine blood concentrations decreased by 31, 28, and 41%, respectively. Portal venous glutamine concentration was not affected by fasting. A glucose [PV-A] was not found in either fed or fasted states. Whereas the lactate [PV-A] was not present in fed rats, it was negative in fasted rats. Alanine [PV-A] was positive in fed and fasted rats. The glutamine [PV-A] was negative in fed and fasted rats. These data indicate that portal venous concentrations of the gluconeogenic precursors, lactate and alanine, decrease in fasted rats. In fasted rats intestinal utilization of lactate increases as reflected by a negative [PV-A]. Fasting did not affect alanine production by the intestine or glutamine utilization. Despite these changes with fasting, we conclude that the intestine does not appear to be able to maintain portal venous blood concentrations of gluconeogenic precursors.

Alanine↗
PubMed1991

Expression of the genes for insulin-like growth factor-I (IGF-I), IGF-II, and IGF-binding proteins-1 and -2 in fetal rat under conditions of intrauterine growth retardation caused by maternal fasting.

Evidence suggests that insulin-like growth factors-I and -II (IGF-I and II) play a role in regulating fetal growth and development. In the fetus, IGF-I and -II are complexed with two specific binding proteins (IGFBP-1 and -2), which are thought to modulate the actions of the IGFs in target tissues. We examined regulation of the genes for IGF-I, IGF-II, IGFBP-1, and IGFBP-2 in fetal rat liver in an experimental model for intrauterine growth retardation caused by maternal fasting on days 17-21 of gestation. The mean weight of fetuses from the fasted dams was 27-32% lower than the mean weight of fetuses from the fed dams. The concentration of immunoreactive IGF-I was decreased by 71% in serum of fetuses from the fasting dams. The concentration of immunoreactive IGF-II was slightly decreased (by 12%) in serum of fetuses from the fasting dams, whereas the concentration of immunoreactive pro-IGF-II E-domain peptide was decreased by 31%. The abundance of hepatic IGF-I mRNA was decreased by 55% in fetuses from the fasting dams. In contrast, the abundance of IGF-II mRNA in fetal liver was not significantly decreased by maternal fasting. Maternal fasting caused a 2-fold increase in the abundance of IGFBP-1 mRNA in fetal liver, whereas it did not change the abundance of IGFBP-2 mRNA. The induction of IGFBP-1 mRNA in liver of the growth-retarded fetuses is similar to the induction that occurs in liver of fasting adults, while the lack of regulation of IGFBP-2 mRNA differs from the strong induction of IGFBP-2 mRNA that occurs in liver of fasting adults. In summary, these results indicate that maternal fasting causes a decrease in fetal IGF-I gene expression, a decrease in fetal serum IGF-I, and a slight decrease in fetal serum IGF-II and pro-IGF-II E-domain peptide concentrations. Maternal fasting also causes an increase in fetal IGFBP-1 gene expression. Changes in fetal insulin and glucose may be related to changes in expression of the IGF-I and IGFBP-1 genes in the growth-retarded fetuses. The decreased expression of IGF-I and -II and increased expression of the IGFBP-1 gene may contribute to the fetal growth retardation observed in this model system.

Animals↗
PubMed1996

Pretreatment with bovine growth hormone is as effective as treatment during metabolic stress to reduce catabolism in fasted lambs.

The effects of recombinant bovine GH (rbGH) treatment on the insulin-like growth factor (IGF) axis and protein metabolism during fasting induced metabolic stress were evaluated in young lambs. To explore whether rbGH pretreatment alone might offer a degree of protection against nutritional stress, we compared the effects of rbGH given only before or during the fasting-induced metabolic stress with that given over the whole period. The animals were fed ad libitum for 5 days (well fed phase) and then fasted for 70 h (fasted phase). The rbGH was administered during either the well fed and the fasted phase (G-G), only during the well fed phase (G-S), or only during the fasted phase (S-G), and the effects were compared with those of saline treatment throughout both phases (S-S; n = 7/group). The rate of net protein catabolism, analyzed on the final day of the study, was reduced (P < 0.001) to a similar degree in all rbGH-treated groups compared with that in the S-S group. rbGH pretreatment was as effective as rbGH administered during the catabolic phase. Plasma IGF-I was increased (P < 0.001) in the well fed phase by rbGH treatment and decreased in the fasted phase in all groups. The rbGH treatment during the fasted phase resulted in a smaller fall in plasma IGF-I levels than saline treatment (P < 0.05, G-G vs G-S and S-G vs. S-S), but no difference was observed in the specific binding of [125I]ovine GH to the hepatic membranes from animals of the different groups. There was a negative correlation between net protein catabolism and plasma IGF-I levels (r = -0.48; P < 0.01) and specific binding of [125I]ovine GH to hepatic membranes (r = -0.56; P < 0.001). Plasma IGF-II levels were decreased by rbGH treatment during the well fed phase, but the responses to treatment during the fasted phase were variable, suggesting that plasma IGF-II is regulated in a different manner than plasma IGF-I. The fasting-induced fall (P < 0.05) in plasma concentrations of IGF-binding protein (IGFBP)-3 was reduced with rbGH treatment, and plasma concentrations IGFBP-2 were altered in an inverse manner. This study suggests that fasting-induced GH resistance can be alleviated by rbGH treatment independent of whether treatment is commenced before or after the onset of catabolic stress. Our observation of prolonged anticatabolic action of prophylactic rbGH treatment supports the proposal that prophylactic use of GH may reduce the degree of catabolism associated with subsequent interventions and, thus, improve clinical outcome.

Animals↗
PubMed2005

Increasing serum betahydroxybutyrate concentrations during the 72-hour fast: evidence against hyperinsulinemic hypoglycemia.

OBJECTIVE: We have determined whether the behavior of betahydroxybutyrate (BOHB) during the 72-h fast of persons without evidence of hyperinsulinemic or any form of organic hypoglycemia might provide indicators of a negative fast. DESIGN: Twenty-one patients with surgically confirmed insulinoma and 34 patients with negative 72-h fasts had BOHB measured every 6 h until Whipple's triad in the former and until 72-h in the latter. RESULTS: Quadratic regression curves of BOHB from the negative fasts showed the typical curve to be flat initially, then increase in a manner that was roughly linear. Using time-specific medians, the changes were: 12-18 h, 0% increase; 18-36 h, 333% increase; 36-54 h, 210% increase, and 54-72 h, 167% increase. In contrast, patients with insulinoma had suppressed BOHB concentrations. Two successive BOHB values in excess of the 18-h level seemed to portend a negative fast. By using the previously published criterion of BOHB more than 2.7 mmol/liter (a surrogate for hypoinsulinemia and thereby an indicator of a negative fast), 74% of persons with a negative fast reached this level before the 72-h point. CONCLUSIONS: Serial measurements of BOHB during the 72-h fast have the potential to provide not only clues during the fast that it will ultimately be negative, but also the opportunity to truncate the fast if the endpoint BOHB criterion for a negative fast is met before 72 h.

3-Hydroxybutyric Acid↗
PubMed1988

Effects of fasting on blood plasma levels, metabolism and metabolic effects of epinephrine and norepinephrine in steers.

Experiments were designed to study effects of 3 days of fasting on blood plasma levels, metabolic clearance rates (MCR) and effects of norepinephrine (NE) and epinephrine (E) on levels of glucose, nonesterified fatty acids (NEFA) and immunoreactive insulin (IRI) in 12 steers. During fasting, levels of E, NE and protein did not change, whereas IRI, T3 and glucose decreased and NEFA, acetoacetate and beta-hydroxybutyrate increased. Before and at the end of fasting, NE or E were iv infused for 120 min. NE and E were elevated after 15 min and to the end of the infusion. The increase in E, but not in NE, was significantly greater after 3 days of fasting than before fasting (P less than 0.05). MCR for E was lower after fasting (299 +/- 17 vs 204 +/- 10 ml.kg-0.75.min-1; P less than 0.001), whereas MCR for NE was not significantly different (455 +/- 37 vs 400 +/- 27 ml.kg-0.75.min-1). MCR was higher for NE than for E, both before and after fasting (P less than 0.05). After the infusion, E and NE decreased within minutes to pre-infusion concentrations. During E infusions, NEFA increased significantly more, whereas glucose increased less in fasted than in fed animals. During NE infusions, NEFA increased in fasted, but not in fed animals, and glucose increased less at the end than before fasting. IRI decreased during E infusions only in fed animals, and transiently increased after the infusion, except after NE infusion in fasted steers.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetoacetates↗
PubMed1998

Analysis of the relationship between fasting serum uric acid and the insulin sensitivity index in a population-based sample of 380 young healthy Caucasians.

AIM: To determine whether fasting serum uric acid is associated with the insulin sensitivity index or with other anthropometric, metabolic or environmental features of the insulin resistance syndrome in a population-based sample of young healthy Caucasians. METHODS: The protocol included 380 unrelated Caucasian subjects (age 18-32 years) who had their insulin sensitivity index and glucose effectiveness measured during a combined intravenous glucose (0.3 g/kg body weight) and tolbutamide (3 mg/kg body weight) tolerance test. A number of anthropometric and biochemical tests, including the level of fasting serum uric acid, were carried out. RESULTS: In univariate analyses the concentration of fasting serum uric acid was negatively correlated to the insulin sensitivity index in both men (r2 = -0.25, P = 0.001) and women (r2 = -0.25, P < 0.001). In multivariate analysis controlling for age, gender, body mass index, waist to hip ratio, maximal aerobic capacity, fasting serum triglyceride and creatinine, daily intake of alcohol, smoking, use of oral contraceptives, and disposition for non-insulin dependent diabetes mellitus, the insulin sensitivity index was not significantly associated with fasting serum uric acid. However, 51% of the variation in the fasting serum uric acid level could be explained, and fasting serum triglyceride was the most important determinant of fasting serum uric acid. CONCLUSION: The major determinant of the fasting serum uric acid level in young healthy Caucasians is the fasting concentration of serum triglyceride, which has been shown to be a biochemical feature of the insulin resistance syndrome. Thus, hyperuricaemia appears to be an indirect part of the insulin resistance syndrome through its association with fasting hypertriglyceridaemia.

Adult↗
PubMed2002

Ghrelin drives GH secretion during fasting in man.

OBJECTIVES: In humans, fasting leads to elevated serum GH concentrations. Traditionally, changes in hypothalamic GH-releasing hormone and somatostatin release are considered as the main mechanisms that induce this elevated GH secretion during fasting. Ghrelin is an endogenous ligand of the GH secretagogue receptor and is synthesized in the stomach. As ghrelin administration in man stimulates GH release, while serum ghrelin concentrations are elevated during fasting in man, this increase in ghrelin levels might be another mechanism whereby fasting results in stimulation of GH release. DESIGN AND SUBJECTS: In ten healthy non-obese males we performed a double-blind placebo-controlled crossover study comparing fasting with and fasting without GH receptor blockade. GH, ghrelin, insulin, glucose and free fatty acids were assessed. RESULTS: While ghrelin levels do not vary considerably in the fed state, fasting rapidly induced a diurnal rhythm in ghrelin concentrations. These changes in serum ghrelin concentrations during fasting were followed by similar, profound changes in serum GH levels. The rapid development of a diurnal ghrelin rhythm could not be explained by changes in insulin, glucose, or free fatty acid levels. Compared with fasting without pegvisomant, fasting with pegvisomant did not change the ghrelin rhythm. CONCLUSIONS: These data indicate that ghrelin is the main driving force behind the enhanced GH secretion during fasting.

Adult↗
PubMed2006

Differential effects of leptin and refeeding on the fasting-induced decrease of pituitary type 2 deiodinase and thyroid hormone receptor beta2 mRNA expression in mice.

Profound changes in thyroid hormone metabolism occur in the central part of the hypothalamus-pituitary-thyroid (HPT) axis during fasting. Hypothalamic changes are partly reversed by leptin administration, which decreases during fasting. It is unknown to what extent leptin affects the HPT axis at the level of the pituitary. We, therefore, studied fasting-induced alterations in pituitary thyroid hormone metabolism, as well as effects of leptin administration on these changes. Because refeeding rapidly increased serum leptin, the same parameters were studied after fasting followed by refeeding. Fasting for 24 h decreased serum T(3) and T(4) and pituitary TSHbeta, type 2deiodinase (D2), and thyroid hormone receptor beta2 (TRbeta2) mRNA expression. The decrease in D2 and TRbeta2 mRNA expression was prevented when 20 mug leptin was administered twice during fasting. By contrast, the decrease in TSHbeta mRNA expression was unaffected. A single dose of leptin given after 24 h fasting did not affect decreased TSHbeta, D2, and TRbeta2 mRNA expression, while 4 h refeeding resulted in pituitary D2 and TRbeta2 mRNA expression as observed in control mice. Serum leptin, T(3), and T(4) after refeeding were similar compared with leptin administration. We conclude that fasting decreases pituitary TSHbeta, D2, and TRbeta2 mRNA expression, which (with the exception of TSHbeta) can be prevented by leptin administration during fasting. Following 24 h fasting, 4 h refeeding completely restores pituitary D2 and TRbeta2 mRNA expression, while a single leptin dose is ineffective. This indicates that other postingestion signals may be necessary to modulate rapidly the fasting-induced decrease in pituitary D2 and TRbeta2 mRNA expression.

Animals↗