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PubMed1992

Preferential retention of linoleic acid-enriched triacylglycerols in liver and serum during fasting.

Fasting has been reported to quantitatively increase linoleic and arachidonic acids in liver triacylglycerols, but the origin and mechanism of this change are unknown. The changes in long-chain fatty acids and triacylglycerol species of liver, serum, adipose tissue, and heart were therefore examined during a period of 24- or 48-h fasting in the rat. In liver and serum triacylglycerols, fasting resulted in a quantitative increase in arachidonic, stearic, linoleic, alpha-linolenic, and docosahexaenoic acids but a decrease in oleic, palmitic, and palmitoleic acids. After fasting, oleic acid was depleted the most from liver and serum triacylglycerols followed by palmitoleic and palmitic acids. Triacylglycerol species containing palmitic, palmitoleic, and oleic acids were depleted the most from liver and serum during fasting. Linoleic acid-enriched triacylglycerol species were proportionally and, in some cases, quantitatively increased in liver and serum triacylglycerols during fasting. Net retention of triacylglycerol species with a total acyl carbon number of 56 or 58 in the liver and 60 in serum was also observed during fasting. Selective retention of triacylglycerol species did not occur in the heart or perirenal or epididymal adipose tissue during fasting. Tissue phospholipid fatty acids were largely unaffected by fasting. Our data suggest that during fasting, long-chain fatty acids released from adipose tissue are differentially utilized and hepatic triacylglycerol species are remodeled, permitting optimal tissue composition of essential fatty acids, particularly linoleic acid.

Adipose Tissue↗
PubMed2003

Effects of one week juice fasting on lipid metabolism: a cohort study in healthy subjects.

OBJECTIVE: We investigated the effects of a popular modified juice fasting program on lipid metabolism. VOLUNTEERS AND METHODS: 5 healthy, nonobese, male volunteers fasted for 8 days. Daily energy intake was limited to 150-300 kcal/d solely as carbohydrates (vegetable and fruit drinks). Physical activity was maintained as before. At baseline, on days 2, 3, and 8 during fasting, and on days 2 and 8 after fasting, serum lipids, lipoproteins, and insulin were investigated. RESULTS: Juice fasting resulted in bi-phasic changes: Until day 2 and 3 triacylglycerols (TG), very low-density lipoprotein apolipoprotein B (VLDL apo B), and insulin decreased by 52, 51, and 65% respectively, while nonesterified fatty acids (NEFA), low-density lipoprotein (LDL) apo B, and LDL cholesterol increased by 363, 38, and 35%. Between day 3 and 8 NEFA increased; TG and insulin increased as well, but remained below baseline values, and LDL cholesterol normalized. After 8 days juice fasting significant changes (p < 0.05) compared to the baseline were found only for free cholesterol (-10%), phospholipids (-14%), apo AI (-9%), apo AII (-11%), insulin (-42%), C-peptide (-57%), and NEFA (+535%, p = 0.0001). Total cholesterol decreased by 9% (n.s.) after 8 days. One week after the ending of fasting all parameters returned to normal. CONCLUSION: Contrary to total fasting and fasting with limited physical activity, 8 days juice fasting without limitation of physical activity results in a decrease of free cholesterol and an only initial increase of LDL cholesterol. After 8 days insulin, TG, and VLDL are still lower than at baseline, however, they have increased compared to the initial phase, probably counterregulatory to a further increase of NEFA.

Adult↗
PubMed1987

Influence of short-term fasting on the pituitary-testicular axis in normal men.

To investigate whether short-term fasting affects serum testosterone (T) in normal subjects, 10 healthy men of normal weight were studied on two occasions: after an overnight fast (8 h), and after an additional 48 h of fasting. Blood glucose declined by 22 +/- 3% between the tests (p less than 0.001). Basal serum T fell from 8.7 +/- 0.7 to 5.7 +/- 0.8 micrograms/l (p less than 0.01), and LH from 6.9 +/- 0.8 to 5.0 +/- 0.7 U/l (p less than 0.01). Serum estradiol (E2) and FSH remained unaffected. To explore possible mechanisms behind the decreased basal release of T and LH, 9 small doses of glucose were given orally at regular intervals during a 56-hour fast to 9 additional normal men to maintain blood glucose levels. These men did not experience a fall in serum T or LH. Six additional normal men were given 50 micrograms GnRH intravenously after an overnight fast, and after a fasting period of 56 h. No acute increase in T was seen after the overnight fast, but after the 56-hour fast GnRH raised serum T by 55 +/- 14% (p less than 0.02). Moreover, fasting augmented the GnRH-induced LH response by 64 +/- 15% (p less than 0.02. These results imply that: short-term fasting exerts inhibitory influence on Leydig cell function via a mechanism which might involve a reduced hypothalamic and/or pituitary stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1970

The effect of fasting, diet, and actinomycin D on insulin secretion in the rat.

The present studies were performed to elucidate the mechanisms responsible for the impairment of glucose-stimulated insulin secretion observed in fasting. Rats fasted for 48 hr displayed marked impairment in their insulin secretory response to both oral and intravenous glucose. Glucose-stimulated insulin secretion was restored within 24 hr by refeeding; actinomycin D given before refeeding blocked the expected return of normal glucose-stimulated insulin secretion despite adequate food intake. Fasted rats refed a diet devoid of carbohydrate failed to display a return of normal insulin secretory responsiveness to oral glucose in contrast to rats fed isocalorically a high carbohydrate diet. Differences in insulin secretion in fed, fasted, and fasted-refed rats could not be attributed to changes in pancreatic insulin content. There was no significant difference in the insulin secretory response to aminophylline of fed, fasted, or fasted-refed rats. The intermittent pulsing of fasted rats with hyperglycemic episodes by the injection of small amounts of glucose (500 mg) intraperitoneally every 8 hr ameliorated the impairment of glucose-stimulated insulin secretion characteristic of the fasting state. These results suggest that the impairment of glucose-stimulated insulin secretion during fasting and its restoration by refeeding are regulated by changes in a glucose-inducible enzyme system in the pancreatic beta cell.

Administration, Oral↗
PubMed1981

Nitrogen sparing induced by leucine compared with that induced by its keto analogue, alpha-ketoisocaproate, in fasting obese man.

We measured the effects of seven consecutive daily infusions of alpha-ketoisocaproate (the alpha-keto analogue of leucine) or leucine itself on urinary urea and total nitrogen excretion during fasting. Two study protocols were undertaken. In protocol I, subjects underwent three separate 14-d fasts: one during which 34 mmol/d of leucine were infused on days 1--7; a second during which 34 mmol/d of alpha-ketoisocaproate were infused on days 1--7; and a third control fast during which no infusions were given. Infusions of alpha-ketoisocaproate significantly reduced daily urine urea nitrogen excretion compared with both the control fasts and the fasts in which leucine was infused (P less than 0.001). This nitrogen-sparing effect of alpha-ketoisocaproate persisted during days 8--14 even though no further infusions were given. Daily urinary urea nitrogen excretion during fasts when leucine was administered did not differ from values observed during control fasts. In protocol II, subjects were starved on two occasions for 14 d. During one fast, infusions of 11 mmol/d of alpha-ketoisocaproate were given on days 1--7; during the control fast, no infusions were given. Daily urine urea nitrogen excretion was lower (P less than 0.001) on days 1--7 and also on days 8--14 of the fast during which alpha-ketoisocaproate was given. The nitrogen-sparing effect of alpha-ketoisocaproate could not be related to changes in circulating levels of amino acids, ketone bodies, or insulin in either protocol. We conclude that alpha-ketoisocaproate infusions decrease the nitrogen wasting of starvation, whereas leucine, studied under identical conditions, does not.

Adult↗
PubMedDate not supplied

Fasting-induced reduction of intestinal reperfusion injury.

BACKGROUND: Fasting is associated with significant structural, functional, and metabolic alterations in the intestinal mucosa. Before abdominal surgery, patients are usually fasted the night before surgery or for a longer period of time if chronic illness is present. The splanchnic organs may experience varying degrees of ischemia/reperfusion as blood vessels are occluded during the various manipulations. METHODS: To study whether fasting alters intestinal reperfusion injury, rats were fasted for 0 to 2 days, and the mesenteric artery was occluded for 30 minutes and then reperfused for 1 hour. Mucosal atrophy was quantitated by measuring jejunal villus height and crypt depth, and mucosal injury was quantitated by measuring jejunal villus width to villus height and mucosal integrity. To determine whether any effect of fasting on reperfusion injury was due to the absence of luminal nutrients or to a systemic nutrient deficiency, rats were fed parenterally for 7 days before ischemia/reperfusion. RESULTS: A 1-day fast produced significant mucosal atrophy. Reperfusion in the 0-day and 1-day fasted animals produced mucosal injury and additional mucosal atrophy. After a 2-day fast, there was no mucosal injury or mucosal atrophy other than that produced by fasting alone. Parenteral feeding before ischemia/reperfusion did not prevent ischemia/reperfusion induced mucosal atrophy and injury. CONCLUSIONS: The protective effect of a 2-day fast before intestinal ischemia/reperfusion cannot be attributed to the physical and chemical absence of food within the intestinal lumen.

Animals↗
PubMed1994

The effect of fasting on insulin-like growth factor-I nuclear transcript abundance in rat liver.

The abundance of insulin-like growth factor I (IGF-I) messenger RNA (mRNA) is decreased in the liver of fasting, protein-restricted, and energy-restricted rats. The extent to which this decrease in steady state mRNA abundance may be attributed to a decrease in IGF-I gene transcription remains unresolved. In the present study, we used an RNase protection assay to quantify IGF-I nuclear transcript (pre-mRNA) and mRNA abundance in whole cellular RNA isolated from liver of fasted and nonfasted male rats (4-6 weeks of age). The results of the RNase protection assay of IGF-I nuclear transcripts were strongly correlated with the results of nuclear transcription elongation (run-on) assays (r > 0.90; P < 0.001). In addition, the RNase protection assay allows for a greater capability for sensitively monitoring gene transcription in a large number of samples. In four different experiments, a consistent decrease in the quantity of IGF-I nuclear transcripts was observed in liver of animals fasted for 72 h, whereas IGF-I pre-mRNA abundance in animals fed ad libitum was highly variable (average intraassay coefficient of variation = 74% vs. 34% for nonfasted and fasted groups). When data from the four experiments were pooled, fasting reduced IGF-I pre-mRNA and mRNA levels by 78% and 70% (P < 0.001), respectively. Fasting also caused a significant decrease in mRNA and nuclear transcript abundance for another nutritionally sensitive gene, the gene encoding transthyretin (TTR). To determine whether the decrease in IGF-I and TTR nuclear transcripts was gene specific, levels of nuclear transcripts for serum albumin, H-ferritin, and ribosomal RNA were also quantified. The results indicated that serum albumin, H-ferritin, and ribosomal RNA nuclear transcripts were not decreased by fasting, demonstrating that the negative effect of fasting was specific for IGF-I and TTR. In summary, these results indicate that IGF-I and TTR nuclear transcripts are specifically decreased by fasting. The decrease in IGF-I mRNA is matched by a similar decrease in IGF-I nuclear transcripts, suggesting that fasting controls IGF-I gene expression primarily at the transcriptional level.

Animals↗
PubMed1981

Reproductive function during fasting in men.

To investigate reproductive function during fasting, six men 20-74% over ideal body weight completed an 18-day study consisting of a 3-day control period, a 10-day total fast, and a 5-day refeeding period. All men lost at least 4.1% of total weight and demonstrated ketonemia and ketonuria. The FSH response to LRH (0.2 microgram/min for 4 h) stimulation was significantly lower (P less than 0.05) during fasting and remained so during refeeding. Serum FSH concentrations were significantly lower (P less than 0.05) during the fast in five of six patients compared to those during the control period, whereas serum LH concentrations were unchanged. The effects of fasting on endogenous LH and FSH pulsations were studied by obtaining serum at 20-min intervals for 6 h on days 2, 11, and 16. Neither the amplitude nor the frequency of LH and FSH pulsations changed significantly during fasting or refeeding. Serum testosterone concentrations were significantly lower (P less than 0.025) by fasting day 9 compared to control values. The 24-h urinary excretion of both LH and FSH increased significantly (P less than 0.05) by fasting day 6 and reached a maximum by fasting day 8. Urinary LH excretion did not return to normal after 3 days of refeeding, whereas urinary FSH excretion returned to baseline by the first day of refeeding. We conclude that during short term fasting in obese men: 1) serum FSH concentrations decrease, 2) the pituitary responsiveness of FSH and LRH is blunted, 3) serum testosterone decreases, and 4) the urinary excretion of both LH and FSH increase.

Adult↗
PubMed1983

Are fasting-induced effects on thyrotropin and prolactin secretion mediated by dopamine?

To investigate whether total caloric deprivation influences TSH and/or PRL responsiveness, seven healthy volunteers fasted overnight (8 h) and were injected iv with a small dose (25 micrograms) of TRH and 30 min later with 40 mg cimetidine (CIM). This combined TRH-CIM test was repeated in the same individuals after a fasting period of 56 h. The TRH-stimulated mean maximal TSH increment fell from 5.1 +/- 1.2 to 1.2 +/- 0.6 microU/ml (P less than 0.01) during fasting. In contrast, both the TRH- and CIM-induced PRL responses were unaffected. To exclude methodologic errors on this reduced TSH responsiveness, an additional four normal subjects fasted for 56 h and then were given TRH alone. Two days later the TRH test was repeated after a fasting period of only 8 h. This experimental design also resulted in a significantly lower TSH response after the longer fasting period than after the shorter period, thus demonstrating that prolonged fasting inhibits TSH responsiveness regardless of whether the starvation period precedes or follows the TRH injection, and regardless of whether the pituitary thyrotrophs are stimulated with TRH plus CIM, or with TRH alone. In an additional seven healthy subjects injected with TRH plus CIM before and after a fasting period of 56 h, a dopamine D-2 receptor blocking agent, metoclopramide (MET), was given orally 90 min before the second TRH-CIM load. This priming with MET failed to restore normal TSH responsiveness in the fasting subjects, thus indicating that the suppressed TSH secretion could not have been mediated through dopamine D-2 receptors. However, since oral pretreatment with MET completely abolished the CIM-elicited PRL response in the fasting subjects, it is reasonable to assume that CIM stimulates PRL release via a reduced dopaminergic inhibition of the pituitary lactotrophs.

Adult↗
PubMed1990

Impaired modulation of hepatic glucose output overnight after a 72-h fast in normal man.

We have previously reported a 25% fall in glucose utilization (Rd) and glucose production (Ra) in normal volunteers during an overnight fast, when glycogenolysis accounts for approximately 70% of hepatic glucose output (HGO). This reduction in Ra and Rd was positively correlated with reductions in glycerol and FFA. To determine if a similar fall in HGO occurs after a prolonged fast when HGO depends solely upon gluconeogenesis, seven normal male volunteers were fasted for 72 h. Glucose kinetics were then assessed overnight using a [3-3H]glucose infusion from 2200-0800 h. Plasma glucose (3.6 +/- 0.1 mM), immunoreactive insulin (2.7 +/- 0.4 mU/L), C-peptide (0.22 +/- 0.03 nmol/l), Rd (1.30 +/- 0.03 mg/kg.min), and Ra (1.28 +/- 0.03 mg/kg.min) were suppressed, and plasma glucagon (98.8 +/- 13.2 pmol/L) was elevated compared to values obtained during the overnight fast, but none of these parameters changed overnight after the 3-day fast. Plasma lactate (0.98 +/- 0.09 mmol/L) and alanine (0.18 +/- 0.03 mmol/L) levels were also unchanged throughout the night. Plasma glycerol (0.14 +/- 0.03 mmol/L) and FFA (0.98 +/- 0.07 mmol/L) were significantly elevated compared to values during the overnight fast, but failed to fall during the study as had been observed during a 14-h fast. We conclude that the modulation of HGO observed during an overnight fast does not occur during prolonged fasting. The lack of nocturnal modulation of HGO when plasma FFA and glycerol levels are fixed at elevated concentrations supports a role of FFA and/or glycerol in the modulation of HGO during an overnight fast.

Adult↗
PubMed1994

Fasting affects serum insulin-like growth factors (IGFs) and IGF-binding proteins differently in patients with noninsulin-dependent diabetes mellitus versus healthy nonobese and obese subjects.

In the present study we have 1) assessed how differences in insulin and GH status between obese patients with noninsulin-dependent diabetes mellitus (NIDDM) and healthy obese (OB) and nonobese (NOB) subjects are associated with different responses of insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) to fasting, and 2) determined whether the IGF-I response to fasting in healthy subjects is secondary to changes in IGFBP-3. In patients with NIDDM, there was a lack of response of serum IGF-I concentrations to 4 days of fasting, contrasted with the significant decrease in IGF-I concentrations in NOB subjects (37%; P < 0.001) and the delayed and attenuated decrease in OB subjects (23%; P < 0.01). Insulin and the insulin-regulated IGFBP-1 were also unchanged during fasting in NIDDM, whereas insulin was decreased and IGFBP-1 was increased in both NOB and OB subjects. Insulin-resistant NIDDM patients, with high basal glucose and insulin, normal IGFBP-1, and low GH, had decreased prefasting serum IGF-I concentrations, similar to the values in fasted body mass index- and age-matched OB subjects. IGFBP-3, the major determinant of the IGF-I turnover rate in serum, was unchanged by fasting, as determined by RIA and Western ligand blot analysis. In accordance, no induction of IGFBP-3 proteolytic activity by fasting could be demonstrated. Serum IGF-II concentrations were also unchanged by fasting. Basal immunoreactive IGFBP-3 levels did not differ among the groups, whereas IGFBP-3 by Western ligand blot analysis was decreased in NIDDM in accordance with the finding of increased IGFBP-3 proteolysis in NIDDM. In conclusion, 1) differences in GH status and modulation of GH induction of IGF-I by insulin resistance could contribute to low basal IGF-I levels and lack of a IGF-I response to fasting in patients with NIDDM; and 2) the turnover rate of IGF-I in serum, which is largely determined by IGFBP-3, is not likely to be altered by short term fasting, suggesting that the decrease in serum IGF-I concentrations is a result of decreased IGF-I production.

Adult↗
PubMed1996

Metabolic effects of triiodothyronine replacement during fasting in obese subjects.

The adaptation to fasting reduces muscle protein breakdown by switching from a carbohydrate to fat fuel economy in normal man. With the discovery of T3 and the observation that its formation from T4 was reduced significantly during starvation, it was proposed that T3 mediated many of these changes. To examine this possibility, otherwise healthy, obese subjects were fasted for 10 days and supplemented with T3 the last 3 days of the fast to bring circulating T3 levels within normal prefasting (weight maintenance) levels. The effects of the same dose of T3 for 3 days were tested during the last 3 days of a 10-day weight maintenance diet for comparison. Both metabolic rate and CO2 production decreased as expected with fasting and did not increase after T3 supplementation. Hepatic glucose appearance rates fell with fasting and increased significantly during T4 supplementation, but not to prefasting levels. Urinary urea nitrogen excretion decreased significantly with fasting and decreased further with T3 supplementation. Lysine appearance did not change during fasting or T3 supplementation, but leucine appearance decreased with T3 supplementation during fasting. These observations suggest that the fall in serum T3 during fasting may not mediate the observed decreases in protein breakdown that occur during fasting and prolonged starvation, but may instead initiate the fall in hepatic glucose appearance.

Adult↗
PubMed1997

Thyrotropin levels during hydrocortisone infusions that mimic fasting-induced cortisol elevations: a clinical research center study.

Both short term fasting and administration of high doses of glucocorticoids lead to marked suppression of serum TSH levels in healthy subjects. However, it is not known whether the more mild serum cortisol elevations seen during fasting can account for fasting-induced TSH suppression. To study this question, eight healthy subjects each underwent three 2-day studies: 1) baseline (adlibitum diet), 2) fasting (56 h of total caloric deprivation), 3) hydrocortisone (HC) infusions at a dose and pulsatile pattern that reproduced cortisol levels measured during each subject's fasting study. Subjects required 34-46 mg HC/24 h to achieve these cortisol levels. During each study, blood samples were drawn every 15 min during the final 24 h for serum cortisol and TSH levels. A TRH stimulation test was performed at the end of each study. By design, fasting and HC infusions induced similar mild increases in 24-h serum cortisol levels (32% over baseline), with the most significant increases seen between 1400-0200 h. Fasting decreased 24-h mean and pulsatile TSH levels 65% from baseline, whereas HC infusions decreased mean and pulsatile TSH levels 51% from baseline. Daytime (0800-0200 h) TSH levels were identical in the two studies, whereas nocturnal (0200-0800 h) TSH levels during HC infusions fell midway between baseline and fasting studies. Serum total T3 and TSH responses to TRH were decreased to a similar degree by fasting or HC infusions. These results suggest that mild elevations in endogenous cortisol levels may mediate at least in part fasting-induced changes in TSH secretion and thyroid hormone levels. In addition, these data show that near-physiological doses of HC and resulting changes in serum cortisol levels within the normal range can cause significant decreases in serum TSH levels.

Adult↗
PubMed1998

Dual regulation of insulin-like growth factor binding protein-1 levels by insulin and cortisol during fasting.

Insulin-like growth factor (IGF) binding protein-1 (IGFBP-1) gene transcription is known to be inhibited by insulin in vivo and in vitro. Levels of IGFBP-1 typically rise during fasting but also rise after acute hypoglycemia, including that induced by insulin, through an unknown mechanism that may involve counterregulatory hormones such as cortisol. To study the regulation of IGFBP-1 secretion during fasting, we measured IGFBP-1, insulin, cortisol, GH, and glucose during the course of standardized fasting studies in a total of 21 children. The fasting studies lasted 13-32 h and were terminated for a whole-blood glucose concentration of less than 50 mg/dL (2.8 mmol). Of the children studied, 9 children had no disorder, 8 had ketotic hypoglycemia, 2 had isolated GH deficiency, and 2 had fatty acid oxidation disorders. During fasting, IGFBP-1 rose above the mean baseline levels of 28+/-5 ng/mL to a mean level+/-SEM of 336+/-59 ng/mL at the time of hypoglycemia (P=0.001). IGFBP-1 was strongly associated with serum insulin and cortisol levels over the entire course of fasting (P < 0.0001)). The interaction of the 2 hormones across time was also strongly significant (P < 0.0001). There was no statistically significant association between IGFBP-1 and GH or glucose. At the time of hypoglycemia, insulin levels were suppressed to 1.7 microU/mL or less, and there was no correlation between IGFBP-1 levels at the end of fasting and final insulin level. In contrast, cortisol levels correlated with IGFBP-1 in the final hypoglycemic sample (r=0.56, P < 0.01). Partial correlation analysis revealed that the relationship between IGFBP-1 and cortisol was unchanged when the data was controlled for insulin levels. These data show that insulin and cortisol both regulate IGFBP-1 secretion during fasting; the effects of insulin and cortisol are strong during the course of fasting. Significant hypoglycemia stimulates a further rise in IGFBP-1, which seems to be regulated, in part, by cortisol. The cortisol-induced rise in IGFBP-1 during fasting and during hypoglycemia potentially serves to prevent the hypoglycemic effects of free IGFs.

Child↗
PubMed2000

Forty-eight-hour fast: the diagnostic test for insulinoma.

Insulinoma causes fasting hypoglycemia due to inappropriate insulin secretion. Its diagnosis is based on demonstrating Whipple's triad during a supervised 72-h fast. For 75 yr, the 72-h fast has been the cornerstone for the diagnosis; however, it has never been critically assessed using newer assays for insulin, C peptide, and proinsulin. Thus, the aim of the current study is to assess the need for a full 72-h fast for the diagnosis of insulinoma. Patients with suspected hypoglycemia with documented glucose concentrations below 45 mg/dL were admitted to the NIH. Data obtained during the supervised fast of patients with pathologically proven insulinoma over a 30-yr period (1970-2000) were reviewed. We identified 127 patients with insulinoma. The average age of patients was 42.7 +/- 15.9 yr, with a predominance of females (62%). 107 patients had a benign tumor, 20 had malignant insulinoma, and 15 patients had multiple endocrine neoplasia type 1. The fast was terminated due to hypoglycemia in 44 patients (42.5%) by 12 h, 85 patients (66.9%) by 24 h, and 120 (94.5%) by 48 h. Seven patients fasted beyond 48 h despite subtle neuroglycopenic symptoms and glucose and insulin concentrations diagnostic of insulinoma. Immunoreactive proinsulin was elevated at the beginning of the fast in 90% of 42 patients. Proinsulin in noninsulinoma, in contrast to insulinoma, patients is usually suppressible; therefore, samples taken in the suppressed state have the greatest diagnostic value. We conclude that with the current available insulin and proinsulin assays, the diagnosis of insulinoma can be made within 48 h. Thus, the 48-h fast should replace the 72-h fast in textbooks and hospital protocols as the new diagnostic standard.

Adolescent↗
PubMed2002

Free and total insulin-like growth factor (IGF)-I levels decline during fasting: relationships with insulin and IGF-binding protein-1.

We have previously demonstrated that IGF-binding protein-1 (IGFBP-1) levels rise steadily during fasting, following an inverse relationship with insulin. The function of the IGFBP-1 rise is unknown, but it has been hypothesized that IGFBP-1 serves as a glucose counterregulatory hormone during fasting and hypoglycemia by binding free IGFs, thus inhibiting IGF interactions with IGF receptors. Our objective in this study was to determine levels of free and total IGFs during fasting together with their interrelationships with simultaneous IGFBP-1, insulin, and glucose levels. Our patient population consisted of 22 children, aged 6 months to 15 yr, who underwent diagnostic fasting studies in the General Clinical Research Center. Blood was sampled at baseline and at 6-h intervals for glucose, IGFBP-1, free and total IGF-I, and insulin. The fasting studies lasted 14-40 h and were terminated at a glucose concentration of less than 50 mg/dl (n = 11) or for the completion of the allotted fasting duration (n = 11). Of the children studied, 11 had ketotic hypoglycemia, 8 had no disorder, 2 had steroid-induced adrenal suppression, and 1 had recovered transient hyperinsulinism. During fasting, IGFBP-1 levels rose above mean initial levels of 27.1 +/- 13.4 ng/ml to a mean of 318.4 +/- 29.9 ng/ml at the end point (P < 0.001). Insulin levels declined from a mean initial level of 7.4 +/- 1.3 mU/ml to a mean level of 1.4 +/- 0.4 mU/ml at the end point (P < 0.001). Concomitantly, free and total IGF-I levels declined from initial levels of 0.48 +/- 0.08 and 180.3+/- 27 ng/ml, respectively, to mean levels of 0.10 +/- 0.02 ng/ml (P < 0.001) and 119.3 +/- 22 ng/ml (P = 0.001), respectively, at the end point. Levels of free IGF-I were inversely associated with IGFBP-1 over the course of fasting (P = 0.002). Similarly, total IGF-I was negatively associated with IGFBP-1 (P = 0.01). We conclude that free and total IGF-I levels decline steadily over the course of fasting. This decline in free IGF-I appears to be the result of the steady rise in IGFBP-1 that occurs as insulin declines. We speculate that the decline in IGF levels, controlled by the rise in IGFBP-1, serves to protect against possible insulin-like activity of the IGFs during fasting.

Adolescent↗
PubMed2000

Fasting exacerbates acute pancreatitis by occlusion of the common bile duct in rats.

We examined the effects of fasting and non-fasting on gallstone-related acute pancreatitis by the occlusion of the common bile duct (OCD). We prepared a rat OCD-induced pancreatitis model under both fasting and non-fasting conditions, and we measured amylase activity in ascites as well as production of inflammatory cytokines and chemokines. We also examined the pathology of the pancreas, myeloperoxidase (MPO) activity in some tissues and mortality rates. In the fasted OCD group, ascites containing a large amount of amylase, interleukin 1beta (IL-1beta), interleukin 6 (IL-6), and cytokine-induced neutrophil chemoattractant-1 (CINC-1) as well as marked hemorrhage and necrosis of the pancreatic acinar cells were observed. Pulmonary MPO activity increased 3.4-fold compared to the control group. In the non-fasted OCD group, there was no development of ascites. Slight necrosis of acinar cells and slight increases in pulmonary MPO activity were observed. In addition, in the fasted OCD group, the cumulative mortality rate was 50% 6 days after ligation. However, in the non-fasted OCD group, none of the animals died. These results suggest that gallstone-related severe pancreatitis depends on fasting-related structural and/or functional changes in the pancreas. Moreover, increased production of inflammatory cytokines and chemokines in ascites under fasting condition may be involved in multiple organ failure resulting from severe acute pancreatitis.

Acute Disease↗
PubMed1997

Effects of long-term total fasting and insulin on ob gene expression in obese patients.

In the present study the effect of long-term fasting (6 days) on obese (ob) gene expression was examined in nine severely obese females of 34 +/- 3 years and with a body mass index of 46.4 +/- 2.3 kg/m2. Six days of fasting induced a significant weight loss (126.8 +/- 5.3 vs 120.5 +/- 5.1 kg, P < 0.0001). Insulin-stimulated glucose uptake (hyperinsulinemic, euglycemic clamp, insulin infusion rate 1.5 mU/kg per min) was markedly reduced following fasting (M-value 5.96 +/- 0.74 vs 2.79 +/- 0.23 mg/kg per min, P < 0.0001). Ob mRNA/beta-actin concentration in fat biopsies from abdominal subcutaneous adipose tissue was unchanged after 6 days of fasting (1.50 +/- 0.40 vs 1.47 +/- 0.36 arbitrary units, not significant), whereas serum leptin levels decreased significantly from 53.8 +/- 4.7 to 30.7 +/- 2.0 ng/ml (P < 0.0001) during the same period. No significant correlations were found between insulin-stimulated glucose uptake and serum leptin concentration, either prior to the fast or after the fast. Serum leptin levels were unchanged by hyperinsulinemia for 3 h during the clamp prior to the fast, while hyperinsulinemia for 3 h after 6 days of fasting increased serum leptin by 25% (P < 0.01). In conclusion, 6 days of fasting reduced serum leptin by about 40%. In contrast, ob mRNA in abdominal subcutaneous adipose tissue was unchanged. Furthermore, after 6 days of fasting insulin was able to increase the serum level of leptin significantly, indicating that the effect of insulin on the level of leptin is dependent on the nutritional state.

Adipose Tissue↗