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PubMed1992

Augmented growth hormone (GH) secretory burst frequency and amplitude mediate enhanced GH secretion during a two-day fast in normal men.

Serum GH concentrations are increased in fasted or malnourished human subjects. We investigated the dynamic mechanisms underlying this phenomenon in nine normal men by analyzing serum GH concentrations measured in blood obtained at 5-min intervals over 24 h on a control (fed) day and on the second day of a fast with a multiple-parameter deconvolution method to simultaneously resolve endogenous GH secretory and clearance rates. Two days of fasting induced a 5-fold increase in the 24-h endogenous GH production rate [78 +/- 12 vs. 371 +/- 57 micrograms/Lv (Lv, liter of distribution volume) or 0.24 +/- 0.038 vs. 1.1 +/- 0.16 mg/m2 (assuming a distribution volume of 7.9% body weight), P = 0.0001]. This enhanced GH production rate was accounted for by 2-fold increases in the number of GH secretory bursts per 24 h (14 +/- 2.3 vs. 32 +/- 2.4, P = 0.0006) and the mass of GH secreted per burst (6.3 +/- 1.2 vs. 11 +/- 1.6 micrograms/Lv, P = 0.002). The latter was a result of increased secretory-event amplitudes (maximal rates of GH release attained within a burst) with unchanged secretory burst durations. GH was secreted in complex volleys composed of multiple discrete secretory bursts. These secretory volleys were separated by shorter intervals of secretory quiescence in the fasted than fed state (respectively, 88 +/- 4.2 vs. 143 +/- 14 min, P = 0.0001). Similarly, within volleys of GH release, constituent individual secretory bursts occurred more frequently during the fast [every 33 +/- 0.64 (fasted) vs. every 44 +/- 2.0 min (fed), P = 0.0001]. The t1/2 of endogenous GH was not significantly altered by fasting [18 +/- 2.2 (fasted) vs. 20 +/- 1.5 min (fed), P = 0.47]. Serum insulin-like growth factor I concentrations were unchanged after 56 h of fasting. In conclusion, the present data suggest that starvation-induced enhancement of GH secretion is mediated by an increased frequency of GHRH release, and longer and more pronounced periods of somatostatin withdrawal.

Adult↗
PubMed1997

Fasting and postprandial lipid abnormalities in hypopituitary women receiving conventional replacement therapy.

Hypopituitary patients, particularly women, have excess mortality, mostly due to vascular disease. We have studied circulating lipid and lipoprotein concentrations, fasting and over 24 h, in hypopituitary women and men and in matched controls. Firstly, 67 hypopituitary patients (36 women) and 87 normal controls (54 women) were studied after an overnight fast. Secondly, 12 patients (6 women) and 14 matched controls (7 women) were studied over 24 h of normal meals and activity. The patients were all GH deficient and were replaced with cortisol, T4, and sex hormones where appropriate, but not with GH. In the first study, circulating triglycerides, total cholesterol, high density lipoprotein (HDL) cholesterol, and low density lipoprotein (LDL) cholesterol were measured after an overnight fast. In the second study, fasting levels of apolipoprotein B, apolipoprotein A1, and lipoprotein(a) were also measured, and then circulating triglyceride and total cholesterol concentrations were measured over 24 h. Fasting concentrations of triglyceride (mean +/- SEM, 1.73 +/- 0.22 vs. 1.11 +/- 0.09 mmol/L; P = 0.0025), total cholesterol (6.45 +/- 0.25 vs. 5.59 +/- 0.21 mmol/L; P = 0.002), LDL cholesterol (4.58 +/- 0.24 vs. 3.80 +/- 0.19 mmol/L; P = 0.007), and apolipoprotein B (135 +/- 10 vs. 111 +/- 9 mg/dL; P = 0.048) were elevated in hypopituitary compared to control women. The lipid alterations were observed in older and younger women and occurred independently of sex hormone or glucocorticoid replacement. Fasting values were not significantly different in hypopituitary and control men. Patients and controls (women and men) had similar fasting HDL cholesterol, apolipoprotein A1, and lipoprotein(a) concentrations. Although the differences that existed in fasting lipid values were most marked in women, the men were also abnormal in this respect, in that a higher proportion of hypopituitary than control men had total and LDL cholesterol above recommended values (> or = 6.2 and > or = 4.1 mmol/L, respectively). In the postprandial period (0730-2030 h), the areas under the curve (AUC) for circulating triglyceride and total cholesterol were significantly higher in hypopituitary than control women (P = 0.0089 and P = 0.0016, respectively). The AUC for triglyceride and total cholesterol over 24 h were also significantly increased (P = 0.009 and P = 0.0004, respectively). No significant differences were observed for postprandial and 24-h AUC for triglyceride and total cholesterol concentrations in men. We conclude that hypopituitarism with conventional replacement therapy is associated with unfavorable fasting and postprandial lipid and lipoprotein concentrations, particularly in women. The changes may contribute to the observed increased vascular morbidity and mortality.

Adult↗
PubMed2000

Short-term fasting selectively suppresses leptin pulse mass and 24-hour rhythmic leptin release in healthy midluteal phase women without disturbing leptin pulse frequency or its entropy control (pattern orderliness).

Nutritional signals strongly regulate neuroendocrine axes, such as those subserving release of LH, GH, and TSH, presumptively in part via the adipocyte-derived neuroactive peptide leptin. In turn, leptin release is controlled by both acute (fasting) and long-term (adipose store) nutrient status. Here, we investigate the neuroendocrine impact of short-term (2.5-day) fasting on leptin release in healthy young women studied in the steroid-replete midluteal phase of the normal menstrual cycle. Eight women each underwent 24-h blood sampling at 10-min intervals during a randomly ordered 2.5-day fasting vs. fed session in separate menstrual cycles. Pulsatile leptin release was quantified by model-free Cluster analysis, the orderliness of leptin patterns by the approximate entropy statistic, and nyctohemeral leptin rhythmicity by cosinor analysis. Mean (24-h) serum leptin concentrations fell by 4.6-fold during fasting; namely, from 15.2+/-2.3 to 3.4+/-0.6 microg/L (P = 0.0007). Cluster analysis identified 13.9+/-1.1 and 14.3+/-1.1 leptin peaks per 24 h in the fed and fasting states (P = NS), and unchanging leptin interpeak intervals (89+/-5.4 vs. 92+/-5.3 min). Leptin peak area declined by 4.2-fold (155+/-21 vs. 37+/-7 area units, P = 0.004), due to a reduction in incremental leptin pulse amplitude (4.4+/-0.7 vs. 1.0+/-0.13 microg/L, P = 0.0011). The cosine amplitude and mesor (mean) of the 24-h leptin rhythm decreased by 4-fold, whereas the acrophase (timing of the nyctohemeral leptin peak) remained fixed. The approximate entropy of leptin release was stable, thus indicating preserved orderliness of leptin release patterns in fasting. Cross-correlation analysis revealed both positive (fed) and negative (fasting) leptin-GH relationships, but no leptin-LH correlations. In summary, short-term (2.5-day) fasting profoundly suppresses 24-h serum leptin concentrations and pulsatile leptin release in the sex steroid-sufficient midluteal phase of healthy women via mechanisms that selectively attenuate leptin pulse area and incremental amplitude. In contrast, the pulse-generating, nyctohemeral phase-determining, and entropy-control mechanisms that govern 24-h leptin release are not altered by acute nutrient restriction at this menstrual phase. Leptin-GH (but not leptin-LH) showed nutrient-dependent positive (fed) and negative (fasting) cross-correlations. Whether similar neuroendocrine mechanisms supervise altered leptin signaling during short-term nutrient restriction in men, children, or postmenopausal women is not known.

Adult↗
PubMed2000

Homeostatic joint amplification of pulsatile and 24-hour rhythmic cortisol secretion by fasting stress in midluteal phase women: concurrent disruption of cortisol-growth hormone, cortisol-luteinizing hormone, and cortisol-leptin synchrony.

Short-term fasting as a metabolic stress evokes prominent homeostatic reactions of the reproductive, corticotropic, thyrotropic, somatotropic, and leptinergic axes in men and women. Although reproductive adaptations to fasting are incompletely studied in the female, nutrient deprivation can have major neuroendocrine consequences in the follicular phase. Unexpectedly, a recent clinical study revealed relatively preserved sex steroid and gonadotropin secretion during short-term caloric restriction in the midluteal phase of the menstrual cycle. This observation suggested that female stress-adaptive responses might be muted in this sex steroid-replete milieu. To test this hypothesis, we investigated the impact of fasting on daily cortisol secretion in healthy young women during the midluteal phase of the normal menstrual cycle. Eight volunteers were each studied twice in separate and randomly ordered short-term (2.5-day) fasting and fed sessions. Pulsatile cortisol secretion, 24-h rhythmic cortisol release, and the orderliness of cortisol secretory patterns were quantified. Within-subject statistical comparisons revealed that fasting increased the mean serum cortisol concentration significantly from a baseline value of 8.0+/-0.61 to 12.8+/-0.85 microg/dL (P = 0.0003). (For Systeme International conversion to nanomoles per L, multiply micrograms per dL value by 28.) Pulsatile cortisol secretion rose commensurately, viz. from 101+/-11 to 173+/-16 microg/dL/day (P = 0.0025). Augmented 24-h cortisol production was due to amplification of cortisol secretory burst mass from 8.2+/-1.5 to 12.9+/-2.0 microg/dL (P = 0.017). In contrast, the estimated half-life of endogenous cortisol (104+/-9 min), the calculated duration of underlying cortisol secretory bursts (16+/-7 min) and their mean frequency (14+/-2/day) were not altered by short-term fasting. The quantifiable orderliness of cortisol secretory patterns was also not influenced by caloric restriction. Nutrient deprivation elevated the mean of the 24-h serum cortisol concentration rhythm from 12.4+/-1.3 to 18.4+/-1.9 microg/dL (P = 0.0005), without affecting its diurnal amplitude or timing. Correlation analysis disclosed that fasting reversed the positive relationship between cortisol and LH release evident in the fed state, and abolished the negative association between cortisol and GH as well as between cortisol and leptin observed during nutrient repletion (P < 0.001). Pattern synchrony between cortisol and GH as well as that between cortisol and LH release was also significantly disrupted by fasting stress. In summary, short-term caloric deprivation enhances daily cortisol secretion by 1.7-fold in healthy midluteal phase young women by selectively amplifying cortisol secretory burst mass and elevating the 24-h rhythmic cortisol mean. Augmentation of daily cortisol production occurs without any concomitant changes in cortisol pulse frequency or half-life or any disruption of the timing of the 24-h rhythmicity or orderliness of cortisol release. Fasting degrades the physiological coupling between cortisol and LH, cortisol and GH, and cortisol and leptin secretion otherwise evident in calorie-sufficient women. We conclude that the corticotropic axis in the young adult female is not resistant to the stress-activating effects of short-term nutrient deprivation, but, rather, evinces strong adaptive homeostasis both monohormonally (cortisol) and bihormonally (cortisol paired with GH, LH, and leptin).

Activity Cycles↗
PubMed2001

Fasting glucose insulin ratio: a useful measure of insulin resistance in girls with premature adrenarche.

The purpose of this study was to determine whether the fasting glucose/insulin ratio is a useful screening test for insulin resistance in prepubertal girls with premature adrenarche. The glucose/insulin ratio was compared with the insulin sensitivity index calculated from the frequently sampled iv glucose tolerance test with tolbutamide using the minimal model computer program. Thirty-three prepubertal girls (22 Caribbean Hispanic and 11 African American; mean age, 6.8 yr; bone age, 8 yr) were studied. All underwent a 60-min ACTH stimulation test. The fasting glucose/insulin ratio was also compared with IGF-binding protein-1 and ACTH-stimulated androgen levels. Insulin sensitivity correlated significantly with the glucose/insulin ratio (0.76; P < 0.001), fasting insulin (0.75; P < 0.001), and IGF-binding protein-1 (0.59; P < 0.005). Stepwise regression analysis with the insulin sensitivity index as the dependent variable showed that the fasting glucose/insulin ratio was significantly predictive of the insulin sensitivity index (P < 0.002). When viewed as a screening test, setting a value of the fasting glucose/insulin ratio of less than 7 as abnormal and of less than 5.7 x 10(-4) min/microU.ml for the insulin sensitivity index as evidence of insulin resistance (normal prepubertal insulin sensitivity index, >5.7 x 10(-4) min/microU.ml), the sensitivity of the fasting glucose/insulin ratio was 87%, and the specificity was 89%. Furthermore, those girls with a low glucose/insulin ratio (<7) had higher body mass index, fasting insulin, free T, and ACTH-stimulated 17-hydroxypregnenolone and lower fasting IGF-binding protein-1 and SHBG than those girls with a glucose/insulin ratio greater than 7. The fasting glucose/insulin ratio is a useful screening test for insulin resistance in prepubertal Caribbean Hispanic and African American girls with premature adrenarche.

Adrenal Cortex Diseases↗
PubMed1996

Effect of the duration of fasting on myocardial fluorine-18-fluorodeoxyglucose positron emission tomography images in normal males.

To evaluate the effect of the duration of fasting on myocardial fluorine-18-fluorodeoxyglucose (FDG) uptake and distribution, 16 FDG-positron emission tomography (PET) studies were performed in 7 normal volunteers under three different conditions: glucose loading, 6 h fasting and overnight fasting. In the glucose-loaded condition, all subjects had good image quality, and myocardial metabolic rates of glucose (MRGlc) were significantly higher than those in the other two conditions. In the 6 h and overnight fasting conditions, image qualities varied according to MRGlc. Although there were visually distinct regional differences with MRGlc ranging from 0.05 to 0.15 mumol/min per g, these differences were not impressive by a quantitative analysis. The ranges of MRGlc in these two fasted conditions overlapped each other. There was a significant negative linear correlation between MRGlc and serum free fatty acid levels. Thus, MRGlc and image quality in fasted normal subjects varied with the extent of the fed-to-starved transition under clinical fasting conditions (6 h to overnight), and this transition does not depend solely on the duration of fasting. These findings may explain the heterogeneity in FDG studies under fasting conditions.

Adult↗
PubMed2002

Different responses of metallothionein and leptin induced in the mouse by fasting stress.

Changes in metallothionein (MT) and leptin under fasting stress were studied. MT content in the liver of mice increased markedly during continuous fasting periods up to 66 h. Hepatic content of MT increased significantly in mice during the first three cycles of alternate daily fasting-feeding, and then the rate of increase gradually decreased with repetition of this cycle. At the end of 10 cycles, the hepatic MT content was still greater in stressed mice than in the control, although the rate of increase decreased. On the other hand, the plasma concentration of leptin decreased dramatically during continuous fasting. The plasma leptin level recovered to the basal level at the end of 10 cycles of fasting-feeding. These data indicate that MT induction was strongly increased, but leptin was scarcely induced under the continuous fasting stress, and that rates of the changes in MT and leptin levels were gradually reduced under the repeated fasting stress, which may result from an inborn tolerance. Fasting presumably causes translocation of zinc from intracellular to extracellular space, from which it is taken into target organs. The increased zinc-bound MT under the continuous fasting may partly result from the need to maintain zinc and protect tissues against oxidative damage.

Animals↗
PubMed1991

Effects of dietary cholesterol and fasting on hamster plasma lipoprotein lipids.

Hamsters are commonly utilized for comparative study of cholesterol metabolism. The present study was conducted to assess the effects of fasting on the plasma lipoprotein cholesterol concentrations of hamsters. Over a period of 3 weeks, adult male Golden Syrian hamsters (n = 32) were fed chow with or without the addition of 2 g/kg cholesterol. Half of the animals consuming each diet were fasted for 18 hours prior to blood sampling. Comparison of diets showed the following increases in those animals receiving cholesterol: total plasma cholesterol (180%) and triacylglycerols (75%), high density (75%), low density (250%), and very low density (560%) lipoprotein cholesterol. Compared with fasted animals, total plasma triacylglycerols were higher in both non-fasted diet groups. Compared with fasted hamsters that had received cholesterol, total plasma cholesterol (mean +/- SE mmol/l) was greater (6.36 +/- 0.18 vs 5.43 +/- 0.21; p less than or equal to 0.05) in the non-fasted group, due primarily to higher VLDL cholesterol (2.07 +/- 0.18 vs 1.58 +/- 0.18; p less than or equal to 0.05). There were no differences in HDL cholesterol (2.07 +/- 0.05 vs 2.17 +/- 0.08) or LDL cholesterol (1.29 +/- 0.08 vs 1.37 +/- 0.05) between fasted and non-fasted hamsters fed cholesterol. Fasting is not necessary for the study of the plasma HDL cholesterol and LDL cholesterol of hamsters fed cholesterol.

Animals↗
PubMed1999

Acute fasting diminishes the circadian rhythm of biochemical markers of bone resorption.

OBJECTIVE: Biochemical markers of bone turnover exhibit circadian rhythms with the peak during the night/early morning and the nadir in the late afternoon. The nocturnal increase in bone resorption could theoretically be caused by the absence of food consumption which brings about a decrease in net calcium absorption and an increase in parathyroid hormone (PTH), followed by increased bone resorption in response to the body's demand for calcium. The aim of the present study was to assess the influence of a 33-h fast on the circadian variation in biochemical markers of bone turnover. DESIGN: Eleven healthy premenopausal women (age: 24+/-5 years) participated in a randomised, cross-over study consisting of two periods: either 33h of fasting (fasting) followed 1 week later by a 33-h period with regular meals eaten at 0800-0830h, 1130-1230h and 1800-1900h (control) or vice versa. METHODS: Urinary CrossLaps (U-CL/Cr) corrected with creatinine, as a marker of bone resorption; serum osteocalcin (sOC) as a marker of bone formation; serum intact PTH (iPTH); serum phosphate; and serum calcium corrected with albumin. RESULTS: Both the fasting and the control periods showed a significant circadian rhythm in U-CL/Cr (P<0.001), but the decrease was significantly less pronounced in the morning hours during the fasting period. Fasting resulted in a significant decrease in serum iPTH (throughout the study period) as compared with the control period (P<0.05-0.001). No change was observed in sOC by fasting. CONCLUSION: Food consumption has a small influence on the circadian variation in bone resorption, independent of PTH. The fall in iPTH during fasting may be secondary to an increased bone resorption produced by fasting.

Adult↗
PubMed2000

Changes in renal tri-iodothyronine and thyroxine handling during fasting.

OBJECTIVE: Liver handling of thyroid hormones (TH) has been known to alter significantly during fasting. This study investigates whether renal handling of TH is also changed during fasting. METHODS: We measured urinary excretion rates and clearances of free tri-iodothyronine (T(3)) and free thyroxine (T(4)) in healthy subjects prior to and on the third day of fasting. RESULTS: During fasting, both mean T(3) and T(4) urinary excretion decreased significantly to a mean value of 42% of control. Also, total and free (F) serum T(3) concentrations declined significantly, but serum T(4) did not change. Both FT(3) and FT(4) clearance decreased significantly during fasting (62% and 42% of control). The fasting-induced decrease in uric acid clearance correlated well with the decrease in FT(3) clearance (r=0.94; P<0.001). Serum concentrations of non-esterified fatty acids (NEFA) were significantly elevated during fasting. CONCLUSIONS: The findings cannot be fully explained by the fasting-induced decrease in serum T(3), and are in accordance with inhibition of uptake of T(3) and T(4) at the basolateral membrane of the tubular cell. This inhibition may be caused by a decreased energy state of the tubular cell and by other factors such as ketoacidosis and/or increased NEFA concentrations during fasting.

Adult↗
PubMed2005

Mini-Mental State Examination is superior to plasma glucose concentrations in monitoring patients with suspected hypoglycaemic disorders during the 72-hour fast.

OBJECTIVE: To determine whether systematic evaluation of cognitive function by the Mini-Mental State Examination (MMSE) allows the objective detection and documentation of cognitive deterioration in patients referred for evaluation of suspected hypoglycaemic disorders by the 72-h fast. DESIGN: Prospective case series. METHODS: In 50 patients referred for evaluation of suspected hypoglycaemic disorders, the MMSE score (maximum 30 points) was assessed at the start and at the end of the fast. RESULTS: The fast was terminated before 72 h in 14 patients because they developed neuroglycopenic symptoms due to hypoglycaemic disorders. Their MMSE score fell from a median of 29 points (range 20-30) at the beginning to 17 points (range 0-24) at the termination of the fast. The score dropped by > or =6 points in all patients with hypoglycaemic disorders. Median (range) plasma glucose concentration at the end of the fast was 2.1 (1.1-2.5) mmol/l. Thirty-six individuals developed no neuroglycopenic symptoms throughout the 72-h fast, their MMSE score remained between 27 and 30 throughout the fast and their median plasma glucose concentration dropped to 2.9 (2-3.6) mmol/l. CONCLUSIONS: Systematic evaluation of cognitive function by the MMSE at the beginning and at the termination of the fast allows objective determination and documentation of the deterioration of the cognitive state in patients with hypoglycaemic disorders. A decline in the cognitive performance by > or =6 points in the MMSE score rather than a distinct plasma glucose concentration should be used as the criterion to terminate the prolonged fast before 72 h.

Adolescent↗
PubMed2003

Effect of desirable fasting triglycerides on the postprandial response to dietary fat.

BACKGROUND: The National Cholesterol Education Program (NCEP) recently revised the "desirable" fasting triglyceride (TG) to < 150 mg/dL, and levels exceeding 200 mg/dL are defined as "high." METHODS: To evaluate the postprandial response to dietary fat, 50 studies were conducted in nonobese, normocholesterolemic subjects. Following an overnight fast, subjects consumed an oral fat load (70 g/m2), and postprandial triglyceride (ppTG) measurements were assessed at 2, 4, 6, and 8 hours. Subjects were divided by fasting TG cutpoints of 100 and 150 mg/dL. RESULTS: The prevalence of ppTG samples exceeding 200 mg/dL was significantly lower with fasting TG < 100 mg/dL (n = 116) compared with TG 100 to 150 mg/dL (n = 56) (8% versus 25%; p = .004, chi-square analysis). In addition, fasting TG < 100 mg/dL (n = 29) was associated with a reduced mean 4-hour peak ppTG level compared with fasting TG > 100 mg/dL (n = 21) (125 mg/dL versus 249.8 mg/dL; p < .0001). Multiple linear regression analysis identified fasting TG as the most important determinant of the postprandial response after adjustment for other covariates (p = .0005). CONCLUSIONS: Because ppTG-rich lipoproteins contribute to coronary heart disease risk, fasting TG < 100 mg/dL may be a more desirable cutpoint than fasting TG < 150 mg/dL in coronary heart disease risk factor assessment.

Adult↗
PubMed1993

Fasting does not impair insulin-stimulated glucose uptake but alters intracellular glucose metabolism in conscious rats.

Effects of 24-h and 48-h fasting on maximal insulin-stimulated whole-body and muscle glucose uptake, glycogen synthesis, and glycolysis were studied in conscious rats by combining the glucose clamp technique with tracer methods. Fasting decreased body weight and basal plasma glucose, plasma insulin, hepatic glucose output, and glucose clearance (P < 0.05 for all). However, maximal insulin-stimulated whole-body glucose uptake, normalized to body weight, was almost identical in fed, 24-h fasted, and 48-h fasted rats (191 +/- 8, 185 +/- 14, and 182 +/- 5 mumol.kg-1.min-1, respectively; P > 0.7). Similarly, rates of insulin-stimulated glucose uptake by four different skeletal muscles, estimated by the 2-deoxyglucose injection technique, were not different among the three groups. In contrast to glucose uptake, insulin-stimulated whole-body glycolysis was decreased significantly after fasting (36% after 48 h fasting; P < 0.05), whereas insulin-stimulated whole-body glycogen synthesis was increased (44% after 48 h fasting; P < 0.05). In fed rats, glycolysis was the major pathway for glucose metabolism during hyperinsulinemia, accounting for 60 +/- 5% of glucose uptake. This fraction was decreased significantly by fasting (P < 0.01), so that after a 48-h fast, glycolysis accounted for only 40 +/- 3% of insulin-stimulated glucose uptake and glycogen synthesis became predominant pathway, accounting for 60 +/- 3% of whole-body glucose utilization. Whole-body patterns of glucose metabolism during hyperinsulinemia were paralleled by glucose metabolism in individual muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Improvement of basal hepatic glucose production and fasting hyperglycemia of type I diabetic patients treated with human recombinant ultralente insulin.

OBJECTIVE: To test whether a suppertime injection of human ultralente insulin in patients with type I diabetes would result in a larger inhibition of basal hepatic glucose production (HGP) and improvement in fasting and mean daily plasma glucose levels. RESEARCH DESIGN AND METHODS: We studied 16 type I diabetic patients (41 +/- 4 years of age; body mass index [BMI] = 23.3 +/- 0.3 kg/m2; diabetes duration > 3 years) with a crossover protocol of therapy with an intermediate and ultralente insulin. All patients were already treated with three injections per day of regular insulin in addition to intermediate-acting (NPH) insulin at suppertime. After a 14-day run-in period, patients were randomly assigned to treatment with equivalent doses (10.8 +/- 0.8 U, at 1900) of intermediate (Humulin I) or ultralente (Humulin U) insulin. After 1 month of treatment, patients were crossed over. No change of the insulin dosage was performed during the study period. Basal HGP was measured by D-(6,6-2H2)-glucose infusion. Plasma glucose concentration was measured in the fasting state and monitored during the day. RESULTS: Before starting the study period, fasting plasma glucose was 13.4 +/- 1.1 mM and plasma free-insulin was 48.0 +/- 4.8 pM. Daily plasma glucose concentration averaged 10.3 +/- 0.3 mM and the area under the curve (AUC) was 1.41 +/- 0.05 mol/14 h. NPH insulin, given at suppertime for a month, did not induce significant changes in fasting plasma insulin (40.2 +/- 4.8 pM), glucose concentration (14.0 +/- 0.9 mM) or HGP (20.2 +/- 2.2 mumol.kg-1.min-1). Accordingly, no change occurred in the average daily plasma glucose (10.3 +/- 0.3 mM) or AUC (1.41 +/- 0.9 mol/14 h). Glycated hemoglobin also was not affected (8.2 +/- 0.4 vs. 8.2 +/- 0.3%). On the contrary, a 4-week treatment with ultralente insulin, also given at suppertime, was associated with a decline in the basal HGP (16.0 +/- 1.3 mumol.kg-1.min-1), fasting (11.3 +/- 0.9 mM) and average daily (9.4 +/- 0.3 mM) plasma glucose concentrations, and AUC (1.29 +/- 0.07 mol/14 h) of plasma glucose level (all P < 0.05). Glycated hemoglobin was reduced (7.9 +/- 0.4%). In each condition, fasting plasma glucose concentration was correlated with the average daily plasma glucose level (basal = 0.78; intermediate = 0.89; ultralente = 0.62; all P < 0.05), which suggests that ultralente insulin likely induces the improvements of metabolic control through reducing fasting plasma glucose. CONCLUSIONS: Our results suggest that treating type I diabetic patients with ultralente insulin at suppertime provides a better modulation of basal HGP so that lower fasting plasma glucose levels are ensured. The reduction of fasting hyperglycemia is likely to affect positively daily plasma glucose control.

Adult↗
PubMed1999

Risk of diabetes in the new diagnostic category of impaired fasting glucose: a prospective analysis.

OBJECTIVE: To prospectively evaluate progression to diabetes in individuals with impaired glucose regulation as defined according to fasting glucose alone or an oral glucose tolerance test (OGTT) (i.e., both fasting and postload glucose) to compare the ability of these two screening methods to identify people at high risk of developing diabetes. RESEARCH DESIGN AND METHODS: A working population of 1,245 nondiabetic telephone company employees aged 40-59 years was studied by OGTT in 1980. Participants were classified according to baseline fasting glucose only (as encouraged by the American Diabetes Association [ADA]) or OGTT (as recommended by the 1998 World Health Organization [WHO] consultation). Progression to diabetes was evaluated 11.5 years later according to the 1997 ADA criteria of a fasting plasma glucose level > or =7.0 mmol/l. RESULTS: With the use of the OGTT, baseline prevalence of impaired glucose regulation was substantially higher than that with fasting glucose alone (7.2 vs. 3.2%); the two groups only overlap for 40.9% of the cases because a fairly large number of people with postload hyperglycemia (59.1%) have normal fasting glucose. Progression to diabetes in participants with normal fasting glucose and postload hyperglycemia is significantly more frequent than that of people with normoglycemia (32.5 vs. 7.2%; P < 0.001) and not significantly different from that of people with both fasting and postload hyperglycemia (i.e., 44.0%). However, the former are not identified as being at unusually high risk of diabetes unless an OGTT is performed. When the use of fasting glucose alone or OGTT was validated as a marker of progression to diabetes, sensitivity was substantially higher for the OGTT (33.3 vs. 9.0%) without major differences in specificity (92.6 vs. 97.0%). CONCLUSIONS: These data (the only data so far available in Caucasians) support the viewpoint that for the identification of people at high risk of diabetes, the use of the OGTT should be maintained.

Administration, Oral↗
PubMed1989

Fasting for 72 h decreases the responses of counterregulatory hormones to insulin-induced hypoglycaemia in normal man.

We have evaluated the influence of fasting on the response of counterregulatory hormones to insulin-induced hypoglycaemia. Eight healthy, non-obese volunteers were studied after an overnight fast and again after a 72-h fast period. Levels of blood glucose were higher after overnight fasting (4.59 +/- 0.10 mmol/l) than after 72 h of fasting (3.38 +/- 0.12 mmol/l). Hypoglycaemia was induced by a constant insulin infusion (2.4 mU/kg/min) and clamped between 2.1 and 2.3 mmol/l of glucose by a variable glucose infusion. Hypoglycaemia evoked stimulation of glucagon release after the overnight fast but did not alter release after 72 h of fasting. The response of other counterregulatory hormones were also influenced by the longer fasting period: the normal rise in adrenaline levels during hypoglycaemia was delayed and attenuated and the normal rise in cortisol levels was absent; paradoxically, cortisol levels decreased during hypoglycaemia. Seventy-two hours of fasting, therefore, profoundly alters hormonal responses to hypoglycaemia.

Adult↗
PubMed1982

The interaction of phosphorus nutrition and fasting on the survival time of young chickens acutely exposed to high temperature.

Phosphorus nutrition and fasting are dependent factors which markedly influence the tolerance of young chickens to high temperature. A study was conducted to further characterize the nature of this interaction. Male chicks fed low phosphorus diets and fasted 24 hr exhibited significantly shorter survival time after exposure to acute heat when compared to fasted chicks previously fed adequate dietary phosphorus. When chicks were fasted for 48 hr, the effect of previous diet was considerably more pronounced. These results showed that the effect of low phosphorus nutrition was potentiated by fasting 48 hr which in itself improved survival time over that of chicks fasted 24 hr. The apparent metabolic responses of chicks to heat as indicated by changes in plasma glucose and total ketones were not related to the observed dietary effects. Plasma phosphate (Pi) and calcium (Ca) decreased significantly during heat exposure. The Ca/pi molar ratio was increased significantly at heat induced exhaustion, indicating a relatively greater heat induced change in Pi. From the initiation of heat exposure to heat exhaustion, the percent change in Pi, but not Ca, was similar in all groups despite marked differences in the time within which this occurred. We concluded that the effect of low phosphorus nutrition on heat tolerance of young chickens persists after a 48-hr fast. In addition, the effects of previous diet were somewhat more pronounced in 48-hr fasted chicks when compared to those fasted 24 hr.

Animal Feed↗
PubMed1987

Characterization of different hematological responses during molts induced by zinc or fasting.

Single Comb White Leghorn hens were induced to molt by complete fasting for 11 days (FAST) or feeding a layer ration that contained 20,000 ppm zinc as zinc oxide for 11 days (ZINC). In both cases hens lost approximately 30% of their initial body weight. A control (CON) group was maintained. At 4, 8, 12, 18, and 42 days after initiation of the treatments, total erythrocyte numbers (TRBC), percent packed cell volume (PCV), mean corpuscular volume, hemoglobin (Hb), mean corpuscular hemoglobin (MCHb), and mean corpuscular hemoglobin concentration (MCHC) were determined. Erythrocytes were characterized as reticulocytes, intermediate Stage VII erythrocytes, or mature Stage VIII erythrocytes. The FAST hens exhibited significantly increased PCV through 18 days, which was not exhibited by ZINC hens. The FAST treatment increased TRBC on Days 8 and 12 and decreased TRBC on Day 42 while ZINC decreased TRBC on Day 4 and increased TRBC on Day 12. The FAST hens exhibited decreased Hb on Day 42, as reproduction resumed. Both ZINC and FAST hens exhibited decreased MCHb and MCHC on Day 12. Percentages of reticulocytes were decreased at Day 4 by FAST and increased at Days 8 and 18 by ZINC. Stage VII erythrocytes were decreased on Days 4 and 12 in FAST hens whereas ZINC hens exhibited a decrease on Day 4 and an increase on Days 8 and 18. Concomitantly, FAST hens exhibited an increase in Stage VIII erythrocytes on Days 4 and 12, whereas an increase on Day 4 and decreases on Days 8 and 18 were observed in ZINC hens.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗