Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FASTING”

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

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

At least 1,351 records · Page 75Linked to original sources

The influence of hypoxia on the relative sensitivity of human tumor cells to 62.5 MeV (p-->Be) fast neutrons and 4 MeV photons.

Fast neutrons have been used in the clinical radiation therapy of tumors largely because of experimental evidence that their cytotoxic effects are much less dependent on oxygen levels than those of low-LET photons. The potential therapeutic advantage of fast neutrons based on hypoxia alone can be calculated as the "hypoxic gain factor", which is the ratio of the OERs for the fast-neutron compared to the photon beams. The hypoxic gain factor that is generally anticipated based on studies with established mammalian cell lines is about 1.6. However, surprisingly few studies have examined the influence of hypoxia on the fast-neutron radiosensitivity of human tumor cells of different histological types. For this reason, we have determined the OERs of five human tumor cell lines exposed to 62.5 MeV (p-->Be) cyclotron-generated fast neutrons or 4 MeV photons from a clinical linear accelerator. The OERs for four chemotherapy-naive cell lines, HT29/5, Hep2, HeLa and RT112, were invariably greater for photons than for neutrons, but all of these values were lower than expected on the basis of the previous literature. Despite their low OERs, these cell lines showed hypoxic gain factors that were within the range of 1.31-1.63, indicating that such effects cannot entirely explain the disappointing clinical results obtained with fast neutrons. In contrast, comparison of the surviving fractions at clinically relevant doses (1.6 Gy of neutrons and 2.0 Gy of photons) for these four tumor cell lines suggested that little benefit should result from neutron treatment. Only the cisplatin-resistant OAW42-CP line showed a significant hypoxic gain factor by this method of analysis. We conclude that, at the dose fractions used in clinical radiation therapy, there may not be a radiobiological precedent for higher local control rates after fast-neutron irradiation of hypoxic tumor cells.

Animals↗

Involvement of ovarian steroids and endogenous opioids in the fasting-induced suppression of pulsatile LH release in ovariectomized rats.

The participation of the ovarian steroids and opioid peptides in the suppression of pulsatile LH release during acute fasting was examined in rats. Ovariectomized rats bearing silicone elastomer implants of oestradiol and/or progesterone were fasted for 48 h and subsequently blood samples were taken every 6 min for 3 h. Pulsatile LH release was suppressed after 48 h of fasting in the ovariectomized rats implanted with oestradiol but not in the oil-implanted controls. This suppression was enhanced after the administration of progesterone together with oestradiol. In a second experiment, ovariectomized rats bearing implants of oestradiol or oil were fasted for 48 h and injected s.c. (2.5 mg/kg body weight) with an opioid antagonist, naloxone hydrochloride, immediately before blood sampling. In the fasted oestradiol-treated ovariectomized rats, naloxone was able to prevent the suppression of pulsatile LH release. In the absence of oestradiol, however, naloxone was without effect on LH release in either the fasted or unfasted animals. These experiments indicate that the suppression of pulsatile LH release after 48 h of fasting is dependent upon oestradiol and that endogenous opioids are involved in the suppression.

Animals↗

Effect of fasting on serum insulin-like growth factor-I (IGF-I) levels and IGF-I-binding activity in cockerels.

White Leghorn male chicks of 40 days of age were fasted for 5 days and then refed. Blood samples were collected from these chicks before, during and after fasting and serum levels of GH and insulin-like growth factor-I (IGF-I) and serum IGF-I-binding activity were determined. The fasting-induced reduction in body weight was accompanied by a significant rise in circulating GH and fall in IGF-I, coupled with increased serum IGF-I-binding activity. When pooled serum was chromatographed under neutral conditions, IGF-I binding activity and IGF-I immunoreactivity were mainly associated with a large (M(r) = 150,000) and a small protein (M(r) = 30,000). Fasting induced a marked increase in the IGF-I-binding activity of the 30 kDa IGF-I-binding protein (IGFBP) and refeeding restored activity to the normal levels seen before fasting. Ligand blotting of serum-binding proteins with 125I-labelled IGF-I, after first subjecting the samples to polyacrylamide gel electrophoresis and transfer to nitrocellulose, revealed that four IGFBPs (M(r) = 20,000, 30,000, 35,900 and 41,000) were present in chicken serum, and that the 125I-labelled IGF-I binding of the 30 kDa monomer was increased by fasting and restored to normal by refeeding in agreement with gel filtration profiles of IGF-I-binding activity. Western blot analysis suggested that the 30 kDa IGFBP is homologous to IGFBP-2 found in mammalian blood plasma. The results show that IGFBPs in chicken serum and their responses to fasting are similar to those in mammals.

Animals↗

Differential regulation of insulin-like growth factor binding protein-2 and -4 mRNA in muscle tissues and liver by diabetes or fasting.

The present study was undertaken to investigate the metabolic regulation of insulin-like growth factor binding proteins (IGFBPs) gene expression in muscles from diabetic or fasted rat. The messenger RNA (mRNA) levels for IGFBP-2 and -4 were analysed by solution hybridization in heart, skeletal and smooth muscle and liver from fasted (3 days) and refed (6, 12, 24, 72 h) rats and rats made diabetic with streptozotocin. In aortic intima-media, the mRNA levels for IGFBP-2 and -4 were decreased by diabetes or fasting and were restored gradually by refeeding. The response of IGFBP-4 mRNA to diabetes appeared two days after injection of streptozotocin, while a significant decrease of IGFBP-2 mRNA was found after a diabetes duration of two weeks. Both diabetes and fasting decreased IGFBP-4 mRNA levels in heart muscle and skeletal muscle and refeeding restored mRNA for IGFBP-4 to normal level. IGFBP-2 mRNA was undetectable in heart muscle and skeletal muscle. In liver IGFBP-4 mRNA was abundantly expressed. It was slightly but significantly decreased by fasting and approached normality with refeeding, while no change was found in diabetic liver. In contrast, liver IGFBP-2 mRNA was much lower in amount than IGF-I mRNA and IGFBP-4 mRNA and was sharply elevated by fasting, and decreased by refeeding. In conclusion, 1) both IGFBP-2 and -4 mRNA in various tissues are regulated by diabetes or fasting; 2) the mRNA for IGFBP-2 is metabolically regulated in a discordant, organ-specific manner.

Animals↗

Effects of fasting on endurance exercise.

Early studies agree that fasting is detrimental to overall physical performance and to endurance performance in humans; however, a study in rats reported an ergogenic effect where time to exhaustion was increased by a glycogen-sparing effect of elevated free fatty acids in blood resulting from a 24-hour fast. Later studies on humans have also found a detrimental effect of fasting on exercise endurance, with the exception of 1 study which found no difference. The discrepancy between humans and rats could not be explained by level of glycogen sparing, mode of exercise, duration of the fast, physiological differences or level of training. The intensity of exercise, and a potential placebo effect of fasting, are possible reasons for the conflicting results. Despite reduced endurance performance, fasted humans are able to exercise and maintain blood glucose homeostasis; the specific cause of an earlier onset of fatigue during a single bout of exercise in the fasted state remains unclear.

Energy Metabolism↗

Changes in fasting-induced adrenocortical secretion of cold-acclimated rats.

Effect of cold acclimation on fasting-induced adrenocortical and metabolic responses was studied in rats. The animals were acclimated to cold by exposure to 5 degrees C for 4 weeks. The warm control animals were kept at 25 degrees C for the same period. Fasting for 48 h decreased the body weight to the same extent in warm controls (WC) and cold-acclimated rats (CA). Plasma free fatty acids concentration increased by fasting, but the degree of increase did not differ between WC and CA. Plasma glucose level decreased in WC, while it increased in CA by fasting. Plasma corticosterone level was significantly higher in CA than in WC. Fasting increased the level in both groups, and the extent of increase as assessed by 95% confidence interval was significantly greater in CA as compared with that in WC. The present results indicate that fasting-induced glucocorticoid secretion is potentiated by cold acclimation, suggesting a possible role of this hormone in some metabolic changes in fasting.

Acclimatization↗

Effects of fasting and refeeding on some metabolic characteristics of rat brown adipose tissue.

To investigate the effects of fasting and refeeding on rat interscapular brown adipose tissue (BAT), we determined in vitro oxygen consumption, in vitro lipolysis, DNA content and composition of fatty acid (FA). Fasting decreased the weights of body and BAT, and the DNA content of BAT. Fasting reduced both basal oxygen consumption and basal lipolysis of BAT. Fasting also suppressed the noradrenaline- and glucagon-induced increases in both oxygen consumption and lipolysis of BAT. In both triglyceride and phospholipid FA of BAT the extent of unsaturation was increased by fasting. Refeeding restored all of these parameters to the control level. These observations indicate that fasting reduces both oxygen consumption and lipolysis of BAT, resulting in reduced thermogenesis, while fasting could stimulate BAT in certain phases of its function as observed in FA composition.

Adipose Tissue, Brown↗

Influence of fasting and refeeding on the antilipolytic effect of insulin in human fat cells obtained from obese subjects.

The antilipolytic effect of insulin was investigated in obese subjects before and after 7 days of total fasting, and 1 h after oral refeeding with 100 g glucose. Isolated fat cells were prepared from subcutaneous gluteal adipose tissue and incubated in vitro. Specific insulin receptor binding and insulin inhibition of basal and isoprenaline-stimulated lipolysis were determined. During the fasting period, a 15% increase (P less than 0.05) in high-affinity insulin binding and a concomitant 3-4-fold increase in insulin sensitivity were noted, and there was a marked enhancement of the maximum insulin-induced inhibition of basal lipolysis, from 4 to 10 mumol of glycerol/10(7) cells/2 h. The maximum insulin-induced inhibition of isoprenaline-induced lipolysis was similar before and after fasting, about 10 mumol/10(7) cells/2 h. Glucose refeeding induced a 30% decrease (P less than 0.02) in high-affinity insulin binding and a 20-60-fold decrease (P less than 0.01) in the sensitivity of the antilipolytic effect of insulin under basal conditions and in the presence of isoprenaline. The maximum antilipolytic effect of insulin, however, was not altered by glucose refeeding. Thus, in the basal state, maximum antilipolytic effect was larger after refeeding as compared with that before fasting. The high-affinity insulin binding and insulin sensitivity were significantly lower after refeeding than before fasting. Before the fasting period, neither the insulin binding nor the antilipolytic effect of the hormone was altered by oral glucose. It is concluded that fasting and glucose refeeding are associated with marked alterations in the antilipolytic effect of insulin on human fat cells of obese subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Insulin's effect on Leucine turnover changes during early fasting in the conscious dog.

To study the effects of insulin on leucine turnover during fasting, acute insulin deficiency was induced by the simultaneous infusion of somatostatin and glucagon in conscious dogs fasted 18 h (N = 10) and 48 h (N = 11). Insulin levels during the basal period (before hormone perturbation) were similar in both groups of dogs (12 +/- 3 versus 10 +/- 3 microU/ml, respectively). Glucagon levels were similar in the two groups (94 +/- 9 versus 106 +/- 19 pg/ml). Leucine levels rose from 118 +/- 9 mumol/L to 155 +/- 12 mumol/L as fasting progressed (P less than 0.005). Its rate of appearance also increased by 30% (P less than 0.005) from 3.4 +/- 0.3 to 4.3 +/- 0.4 mumol/kg/min (P less than 0.005), while its clearance remained unchanged. Acute insulin deficiency caused an increase in leucine levels in both 18-h and 48-h-fasted dogs by 55% (to 181 +/- 10 mumol/L) and 45% (to 225 +/- 20 mumol/L), respectively (P less than 0.005). However, while the rate of appearance of leucine remained unchanged in dogs fasted overnight, it rose to 5.1 +/- 0.3 mumol/kg/min (P less than 0.01) in those fasted 48 h. The metabolic clearance rate fell in both groups, although this drop was twice as great in the 18-h group (from 28 +/- 3 to 17 +/- 3 ml/kg/min, P less than 0.005) as in the 48-h group (from 28 +/- 3 to 23 +/- 2 ml/kg/min, P less than 0.005). We conclude that insulin has disparate effects on protein turnover as fasting becomes more prolonged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Responses of leptin to short-term fasting and refeeding in humans: a link with ketogenesis but not ketones themselves.

We investigated the response of leptin to short-term fasting and refeeding in humans. A mild decline in subcutaneous adipocyte ob gene mRNA and a marked fall in serum leptin were observed after 36 and 60 h of fasting. The dynamics of the leptin decline and rise were further substantiated in a 6-day study consisting of a 36-h baseline period, followed by 36-h fast, and a subsequent refeeding with normal diet. Leptin began a steady decline from the baseline values after 12 h of fasting, reaching a nadir at 36 h. The subsequent restoration of normal food intake was associated with a prompt leptin rise and a return to baseline values 24 h later. When responses of leptin to fasting and refeeding were compared with that of glucose, insulin, fatty acids, and ketones, a reverse relationship between leptin and beta-OH-butyrate was found. Consequently, we tested whether the reciprocal responses represented a causal relationship between leptin and beta-OH-butyrate. Small amounts of infused glucose equal to the estimated contribution of gluconeogenesis, which was sufficient to prevent rise in ketogenesis, also prevented a fall in leptin. The infusion of beta-OH-butyrate to produce hyperketonemia of the same magnitude as after a 36-h fast had no effect on leptin. The study indicates that one of the adaptive physiological responses to fasting is a fall in serum leptin. Although the mediator that brings about this effect remains unknown, it appears to be neither insulin nor ketones.

3-Hydroxybutyric Acid↗

Leptin receptor mRNA identifies a subpopulation of neuropeptide Y neurons activated by fasting in rat hypothalamus.

The decline of leptin (Ob protein) concentrations during fasting is implicated as a signal for increasing the expression of the orexigenic peptide neuropeptide Y (NPY) in the hypothalamus. To test the hypothesis that the effects of food intake on arcuate nucleus NPY activation are mediated by leptin, we performed simultaneous triple in situ hybridization colocalization studies to determine whether the subset of NPY neurons that are activated by fasting preferentially expresses the long form of the leptin receptor (Ob-Rb). Thus, mRNAs encoding NPY and pro-opiomelanocortin (POMC) were colocalized in the arcuate nucleus of fed and fasted rats by fluorescence in situ hybridization in combination with isotopic in situ hybridization for Ob-Rb mRNA. In fed animals, 47% of arcuate nucleus neurons containing NPY mRNA also contained Ob-Rb mRNA, compared with 79% of POMC neurons (P < 0.01). After a 2-day fast, the number of arcuate nucleus neurons with NPY mRNA increased 50% (P < 0.05); the number of these that coexpressed Ob-Rb increased twofold (P = 0.013). Furthermore, Ob-Rb mRNA hybridization in individual NPY neurons increased by 64% (P < 0.02). In contrast, the number of POMC neurons that coexpressed Ob-Rb was unchanged. A significant interpretation of these findings is that the NPY neurons that do not express detectable levels of Ob-Rb mRNA are not activated by fasting, whereas the NPY neurons that are activated by fasting are the ones that express Ob-Rb. These data demonstrate a significant physiological difference between NPY neurons that express Ob-Rb and those that do not. The results support the conclusion that the effect of food intake on NPY neurons is mediated by the direct action of leptin via Ob-Rb receptors expressed by these NPY cells. The results also indicate that expression of Ob-Rb is a defining phenotypic characteristic of the subset of arcuate nucleus NPY neurons that are activated by fasting and play a central role in the adaptive response to negative energy balance.

Animals↗

A high fasting plasma insulin concentration predicts type 2 diabetes independent of insulin resistance: evidence for a pathogenic role of relative hyperinsulinemia.

Fasting hyperinsulinemia is a widely used surrogate measure of insulin resistance and predicts type 2 diabetes in various populations. Whether fasting hyperinsulinemia predicts diabetes independent of insulin resistance is unknown. In 319 Pima Indians with normal glucose tolerance, fasting plasma insulin concentration and insulin-stimulated glucose disposal (M) (hyperinsulinemic clamp) were inversely related, but at any given M, there was substantial variation, with some subjects being hyperinsulinemic and others being hypoinsulinemic relative to their degree of insulin sensitivity. In 262 of the 319 subjects followed prospectively over 6.4 +/- 3.9 years, a high fasting plasma insulin concentration was a significant independent predictor of diabetes, in addition to low M and low acute insulin response (AIR) (intravenous glucose challenge). In 161 of the 319 subjects with follow-up measurements of M and AIR (5.1 +/- 3.9 years), a high relative fasting plasma insulin concentration predicted a decline in AIR but not in M before the onset of diabetes. The adjusted fasting plasma insulin concentration was a familial trait (heritability of 0.52) and in a genome-wide scan, there was suggestive evidence of linkage (logarithm of odds score 1.77) to a region on chromosome 3q, which harbors the gene encoding GLUT2. These results provide the first prospective evidence in humans that fasting hyperinsulinemia itself has a primary role in the pathogenesis of diabetes, independent of insulin resistance. Whether amelioration of basal insulin hypersecretion will prevent diabetes remains to be elucidated.

Adult↗

Association of fasting plasma glucose with heart rate recovery in healthy adults: a population-based study.

Diabetes is associated with abnormal autonomic function and increased mortality. Abnormal heart rate recovery after exercise, a measure of autonomic dysfunction, is also associated with increased mortality. The objective of this study was to determine the association of fasting plasma glucose with abnormal heart rate recovery and its prognostic importance in healthy adults. We studied 5,190 healthy adults who did not have medically treated diabetes (mean age 45 years, 39% women), were enrolled in the Lipid Research Clinics' Prevalence Study, and underwent exercise testing. Heart rate recovery was defined as the change from peak heart rate to that after 2 min of recovery; an abnormal value was < or = 42 bpm. All-cause mortality was assessed over 12 years. A total of 504 participants (10%) had impaired fasting glucose, and 131 (3%) had untreated diabetes. An abnormal heart rate recovery was found in 1,699 (33%). Compared with participants who had normal fasting plasma glucose, abnormal heart rate recovery was more common among those with impaired fasting glucose (42 vs. 31%; relative risk, 1.34; 95% confidence interval [CI], 1.20--1.50; P < 0.0001) and those with diabetes (50 vs. 31%; relative risk, 1.61; 95% CI, 1.35--1.92; P < 0.0001). Fasting plasma glucose remained an independent predictor of abnormal heart rate recovery even after adjustment for age, sex, and other confounders (P = 0.0003). An abnormal heart rate recovery added to impaired fasting plasma glucose for the prediction of death. Fasting plasma glucose is strongly and independently associated with abnormal heart rate recovery, even at nondiabetic levels.

Adult↗

Comparison of fasting and 2-hour glucose and HbA1c levels for diagnosing diabetes. Diagnostic criteria and performance revisited.

OBJECTIVE: Nearly two decades ago, the National Diabetes Data Group (NDDG) and the World Health Organization (WHO) Expert Committee on Diabetes Mellitus published diagnostic criteria for diabetes. We undertook this study to compare the performance of three glycemic measures for diagnosing diabetes and to evaluate the performance of the WHO criteria. RESEARCH DESIGN AND METHODS: In a cross-sectional population-based sample of 1,018 Egyptians > or = 20 years of age, fasting and 2-h glucose and HbA1c levels were measured, and diabetic retinopathy was assessed by retinal photograph. Evidence for bimodal distributions was examined for each glycemic measure by fitting models for the mixture of two distributions using maximum likelihood estimates. Sensitivity and specificity for cutpoints of each glycemic measure were calculated by defining the true diabetes state (gold standard) as 1) the upper (diabetic) component of the fitted bimodal distribution for each glycemic measure, and 2) the presence of diabetic retinopathy. Receiver operating characteristic (ROC) curves were constructed to determine the performance of the glycemic measures in detecting diabetes as defined by diabetic retinopathy. RESULTS: In the total population, the point of intersection of the lower and upper components that minimized misclassification for the fasting and 2-h glucose and HbA1c were 7.2 mmol/l (129 mg/dl), 11.5 mmol/l (207 mg/dl), and 6.7%, respectively. When diabetic retinopathy was used to define diabetes, ROC curve analyses found that fasting and 2-h glucose values were superior to HbA1c (P < 0.01). The performance of a fasting glucose of 7.8 mmol/l (140 mg/dl) was similar to a 2-h glucose of 12.2-12.8 mmol/l (220-230 mg/dl), and the performance of a 11.1 mmol/l (200 mg/dl) 2-h glucose was similar to a fasting glucose of 6.9-7.2 mmol/l (125-130 mg/dl). CONCLUSIONS: Optimal cutpoints for defining diabetes differ according to how diabetes itself is defined. When diabetes is defined as the upper component of the bimodal population distribution, a fasting glucose level somewhat lower than the current WHO cutpoint and a 2-h glucose level somewhat higher than the current WHO cutpoint minimized misclassification. When diabetic retinopathy defines diabetes, we found that the current fasting diagnostic criterion favors specificity and the current 2-h criterion favors sensitivity. These results should prove valuable for defining the optimal tests and cutpoint values for diagnosing diabetes.

Adult↗

Low-dose ethanol predisposes elderly fasted patients with type 2 diabetes to sulfonylurea-induced low blood glucose.

OBJECTIVE: It has previously been demonstrated that the risk of hypoglycemia is low among otherwise healthy elderly fasted patients with type 2 diabetes taking oral sulfonylurea medications. Nevertheless, these agents do cause hypoglycemia in clinical practice, suggesting that accompanying factors must typically be present for hypoglycemia to occur. Ethanol is one putative risk factor that has not been evaluated as a mechanism for low blood glucose among sulfonylurea users. We hypothesized that low concentrations of ethanol would reduce blood glucose concentrations in elderly type 2 diabetic patients receiving sulfonylureas during a short-term fast. RESEARCH DESIGN AND METHODS: A total of 10 type 2 diabetic patients, aged 68 +/- 3 years and receiving 20 mg glyburide daily, participated in a prospective double-blind placebo-controlled in-patient study consisting of two 24-h fasts at least 1 week apart. During hours 14 and 15 of the fasting studies, subjects received intravenous infusions of either 4.35 mmol.kg-1.h-1 ethanol (equivalent to one or two alcoholic beverages) or saline placebo in random order. Ethanol, plasma glucose, insulin, and counterregulatory hormones were assessed very 30-60 min during the final 10 h of the fast. RESULTS: Blood ethanol levels peaked at 17 +/- 2 mmol/l (the lower legal limit of intoxication in New Mexico) during the ethanol study. Plasma glucose concentrations did not differ at baseline (placebo 8.5 +/- 1.8 vs. ethanol 8.7 +/- 1.7 mmol/l; P = 0.50), but nadir plasma glucose was lower after the ethanol infusion compared with placebo (4.4 +/- 1.2 vs. 5.0 +/- 1.4 mmol/l; P = 0.01), and the absolute decline in plasma glucose was also greater during the ethanol study than the placebo study (4.7 +/- 0.9 vs. 3.6 +/- 1.2 mmol/l; P = 0.01). Counterregulatory hormone levels were increased during the ethanol study and nonesterified fatty acid concentrations were suppressed compared with the placebo study. CONCLUSIONS: Low doses of ethanol predispose fasted elderly type 2 diabetic patients to low blood glucose during a short-term fast. This may be one of several mechanisms by which sulfonylurea-induced hypoglycemia occurs in elderly patients.

Administration, Oral↗

Heterogeneity in the relationship between ethnicity, BMI, and fasting insulin.

OBJECTIVE: To determine whether the association of BMI and fasting insulin is modified by ethnicity. RESEARCH DESIGN AND METHODS: Non-Hispanic black (black), non-Hispanic white (white), and Mexican-American men and women aged 20-80 years from the Third National Health and Nutrition Examination Survey (1988-1994) were included in this study. Linear regression models with an interaction term were used to test whether ethnicity modified the association between BMI and fasting insulin. RESULTS: Fasting insulin was 19, 26, 20, and 19% higher in black women than white women with BMI levels of <22, 22-24, 25-27, and 28-30 kg/m(2), respectively. These differences between black and white women converged at BMI levels >30 kg/m(2). Mexican-American women had fasting insulin levels that were 17, 22, 20, and 16% higher than those of white women at BMI levels of 25-27, 28-30, 31-33, and >34 kg/m(2), respectively, but were not different in individuals with BMI levels <25 kg/m(2). Adjusting for established risk factors did not attenuate these associations in women. Differences in fasting insulin among men were not as apparent. CONCLUSIONS: These findings suggest that the effect of obesity on insulin sensitivity is different for Americans in ethnic minorities. In black subjects, fasting insulin is higher at lean weight when compared with white and Mexican-American subjects. In Mexican-American subjects, fasting insulin is higher in overweight individuals when compared with white and black subjects. These findings are more pronounced in women than in men. This result reinforces the importance of designing prevention programs that are tailored to meet the needs of specific populations. Investigation of possible explanations for these differences seems warranted.

Adult↗

Effects of fasting on visual flicker fusion.

Two experiments are reported which investigated the effects of fasting on visual flicker fusion (VFF). In Exp. 1 the VFF of 40 undergraduate students, 20 men and 20 women, whose mean age was 22.5 yr., was measured in nonfasting conditions 1 to 2 weeks before and in fasting conditions during the Muslim fasting month of Ramadan. In Exp. 2 the VFF of a comparable group of 15 men and 15 women, whose mean age was 23.2 yr., was measured in a different month in both fasting and nonfasting conditions. Subjects were assigned randomly to these two conditions. Analysis shows that fasting reduced VFF significantly in both experiments. This finding indicates that fasting is likely to reduce perceptual sensitivity. The results were explained in terms of fatigue and physical exhaustion effects produced by fasting.

Adult↗

Short-term metabolic response in wethers to high dietary protein intake prior to fasting.

Twenty crossbred wether lambs (average body weight 38.9 kg) were examined for selected metabolic responses during fasting as affected by dietary protein level prior to fasting. Animals were fed diet analyzed at 10.4 and 20.3% crude protein (diets A and B, respectively) for 3 weeks and then fasted for 7 days. jugular blood samples were collected 4, 28, 52, 76, 100, 124 and 148 hr after the last feeding. Plasma glucose declined (P less than .05) between 4 and 52 hr, after which no further differences in plasma glucose occurred within or between treatment groups. Plasma urea N (PUN) was higher (P less than .05) in lambs fed diet B at 4, 28, and 52 hr postfeeding. In wethers fed diet A, PUN increased (P less than .05) from 28 to 76 hr postfeeding and then declined to prefasting levels. In wethers fed diet B, PUN did not begin to decrease until 76 hr postfeeding and then gradually declined (P less than .05) until the end of the fast. Plasma ammonia N increased (P less than .05) and plasma albumin decreased (P less than .05) during fasting in both treatment groups, but no differences were observed between the two groups in either parameter. The data support the existence of a "glucose-alanine" cycle in that alanine decreased (P less than .05) in both groups whereas glucose remained constant and PUN increased. Together, these factors suggest enhanced gluconeogenesis from amino acids. Increased branch-chain amino acid oxidation may be responsible for the decrease (P less than .05) in total branched-chain amino acids observed during fasting. The higher dietary protein intake of lambs fed diet B apparently afforded some nutritional advantage, since most of the changes observed occurred approximately 24 hr later in these lambs than in those fed the lower protein diet A before fasting.

Amino Acids↗