Refeeding after the late increase in nitrogen excretion during prolonged fasting in the rat.

Recovery of body mass, food intake and body composition was studied in the laboratory rat after the late increase in nitrogen excretion that characterizes prolonged fasting in mammals and birds. The rats lost 43% of their body mass during 13 days of food deprivation. They all regained their prefasting body mass within a shorter period of 11 days of refeeding. These results confirm that the late increase in nitrogen excretion in rats, as in spontaneously fasting birds, is reversible and is a part of the physiological adaptations to long-term food deprivation. Water intake of the rats continuously decreased during fasting, and the animals virtually stopped drinking as protein utilization increased. On refeeding, changes in water intake paralleled those in food intake. The refed rats progressively increased their daily food intake, that was always higher than the prefasting value (8.0-10.4 vs. 6.7% of body mass). The comparison of organ weights between fed and ad lib refed rats of similar body weight indicates that muscle mass was regained earlier than body fat during refeeding. The laboratory rat therefore appears to be a good experimental model to investigate the metabolic and behavioural changes that occur during spontaneous anorexia and refeeding in wild animals.     

Intermittent fasting modulation of the diabetic syndrome in sand rats. II. In vivo investigations

This study deals with the effects of daily intermittent fasting for 15 h upon the development of diabetes in sand rats exposed to a hypercaloric diet. The same pattern of daily intermittent fasting was imposed on sand rats maintained on a purely vegetal diet (control animals). Over the last 30 days of the present experiments, non-fasting animals gained weight, whilst intermittently fasting sand rats lost weight. In this respect, there was no significant difference between control animals and either diabetic or non-diabetic sand rats exposed to the hypercaloric diet. The postprandial glycemia remained fairly stable in the control animals. During a 3-week transition period from a purely vegetal to a hypercaloric diet, the post-prandial glycemia increased by 5.95 ± 1.26 mM (n=6) in diabetic sand rats, as distinct from an increase of only 0.45 ± 0.56 mM (n=6) in the non-diabetic animals. During the intermittent fasting period, the postprandial glycemia decreased significantly in the diabetic animals, but not so in the non-diabetic sand rats. Before the switch in food intake, the peak glycemia at the 30th min of an intraperitoneal glucose tolerance test was already higher in the diabetic than non-diabetic rats. In both the non-diabetic and diabetic sand rats, intermittent fasting prevented the progressive deterioration of glucose tolerance otherwise observed in non-fasting animals. These findings reveal that, at least in sand rats, intermittent daily fasting prevents the progressive deterioration of glucose tolerance otherwise taking place when these animals are exposed to a hypercaloric diet.     

Resting oxygen consumption in rats during food restriction,starvation and refeeding

Oxygen consumption was measured in male rats during starvation and during different regimens of restricted feeding and refeeding after starvation. Changes in oxygen consumption and body mass were mostly parallel, but rats with a very reduced food intake displayed the same reduction in oxygen consumption as starved rats, despite the smaller reduction in body mass. Also, rats fed different amounts of food after starvation had different oxygen consumptions, but displayed the same changes in body mass. Two different refeeding regimens with restricted food amounts either induced a further depression of oxygen consumption (i.e. below starvation oxygen consumption), or a stabilizing of oxygen consumption on the level of starvation. The changes in oxygen consumption during restriction and feeding after starvation indicate that reductions in resting metabolic rate may not always be predicted from either body mass change or food intake.     

Repeated fasting/refeeding elevates plasma leptin without increasing fat mass in rats

It is known that repeated fasting and refeeding increase capacity of fat storage in adipose tissue as an adaptive response to fasting. However, the amount of weight gain in fasted/refed animals falls behind the control level in most rodent studies. Leptin, an adipocyte-derived hormone that impacts on energy homeostasis, may be up-regulated by repeated cycles of fasting and refeeding. In this study, we investigated the adaptive response of leptin to repeated cycles of 1-day fasting and 1-day refeeding for 42 days in rats. The repeated fasting and refeeding (RFR) rats gained less body weight than the controls. Daily food intake of the RFR rats was decreased after Day 16 and remained suppressed. Circulating leptin levels of the RFR rats were significantly elevated at Day 35 compared with the controls and at Day 44 compared with the controls and pair-fed (PF) rats. Leptin mRNA levels of these rats were also significantly increased in retroperitoneal white adipose tissue (RT-WAT) compared with the controls and PF rats. Moreover, hypothalamic proopiomelanocortic (POMC) gene expression was augmented in the RFR rats compared with the controls and PF rats. However, there was no statistical difference in percent visceral fat mass among the experimental groups. Lipoprotein lipase (LPL) mRNA levels of RFR rats were significantly increased in RT-WAT compared with the controls and PF rats. These data indicated that leptin was up-regulated in response to chronic repeated fasting and refeeding cycles without a concomitant increase in adiposity, and the augmented leptin levels were associated with an increase in POMC gene expression, reduced food intake, and diminished body weight gain.     

Absence of post-fast food compensation in the golden hamster (Mesocricetus auratus).

Ad lib food intakes and body weights were measured for hamsters fed one of 4 different diets. Animals were then placed on an intermittent starvation (IS) schedule in which food was available ad lib on alternate days only. Hamsters of both sexes showed little or no post-fast food compensation, i.e., after 24 hr of food deprivation their daily food intake was no greater than their daily intake during baseline testing. These animals lost a large percentage of their initial body weight and many of them died. Other hamsters restricted daily to half-day feeding periods that nearly coincided with the light (L) or dark (D) phases of the illumination cycle also failed to show food compensation; they generally ate no more during D- or L-periods that followed a half day of food deprivation than during D- or L-periods that succeeded a half day of ad lib feeding. These animals lost substantial portions of their initial body weight and many died. Hamsters refed after a 96-hr fast and an 18% loss in body weight also did not increase their food intake substantially above baseline values. In each of these experiments substantial portions of the body weight lost during starvation were not regained during extended ad lib refeeding regimens. These findings contrast strikingly with the behavior of rats tested concurrently; rats showed a dramatic post-fast hyperphagia, rapid recovery of body weight lost during starvation, and a reversal of the normal nocturnal feeding pattern when refeeding began during L-periods. Hamsters' nocturnal rhythms of eating and drinking were remarkably stable in the face of all the experimental manipulations. However, hamsters, as well as rats, were quite effective in compensating for changes in diet density; a 1:1 dilution of a liquid diet produced a prompt doubling in the volume of diet ingested. Impressive but less complete compensation was recorded when solid diets were diluted with inert substances (kaolin, cellulose). Hoarding and perhaps hibernation rather than compensation may have evolved as adaptations to periods of food scarcity. Noncompensation may be related to hamsters' nonresponsiveness to some signal of energy depletion. The possibility of lipogenesis being a rate-limiting step is considered. The desirability of adequate field data as a prerequisite to laboratory analysis of feeding behavior is emphasized.     

Effects of periodic intake of a high-caloric diet on body mass and leptin resistance

The effects of continuous or intermittent access to a high-caloric (HC) diet, always offered in addition to standard chow, on body mass and leptin resistance were analyzed in female C57BL/6J mice. Susceptibility for diet-induced obesity (DIO) was apparent from the marked preference for the HC diet. Continuous HC diet feeding of mice at 4 weeks of age induced leptin resistance within 2 weeks and massive gains in body mass, although with increasing inter-individual variability in the inbred strain considered to be isogenic. In adult mice receiving HC diet for the first time, leptin treatment failed to reduce energy intake first after 11 days of HC diet feeding, but became effective again within 3 days after HC diet withdrawal. In mice with a history of several preceding periods of access to the HC diet totalling >30 days, supplementary HC diet abolished the anorectic effect of leptin treatment within only 3 days and it reappeared not earlier than 11 days after HC diet withdrawal. Thus, in the investigated DIO-prone mouse strain both, the loss of responsiveness to leptin under HC diet and its recovery after HC diet withdrawal strongly depended on the dietary history. Recovery from leptin resistance during periods of intermittent chow feeding was associated with losses of body mass that did not completely compensate for the obesity-inducing effect of the preceding HC diet.     

Developmental and food-access-dependent changes in effector systems activated by leptin

In small mammals leptin reduces fat stores not only by inhibiting food intake but also by disinhibiting metabolic cold defense. Presuming that postnatal age and feeding regime set the conditions for either mode of leptin action, we compared the caloric equivalents of changes in fat mass, metabolic rate (MR) and food intake (FI) induced by 10-day treatments with leptin, in rats treated from postnatal days 7, 15, 25 onward and in adult mice that were free-feeding or food restricted. Whereas MR changes are known to dominate from postnatal days 7-16, changes in MR explained only about 50% and 30% of the leptin-induced changes in fat mass between days 15-24 and days 25-34, respectively. In adult mice of similar body weights, leptin-induced reductions in fat mass under free-feeding conditions were due only to FI decreases but due only to MR increases under food-restricted conditions. Thus, the same leptin treatment induces the same percentage decrease in body fat content by driving the two effectors differently, depending on age and feeding conditions. Consequently, in assessing the effects of leptin under various physiological conditions, short-term measurements of FI or MR alone are not sufficient. Instead, determination of the resultant decreases in total body fat is required.     

低氧运动干预肥胖模型大鼠下丘脑Nesfatin-1和Ghrelin水平

文题释义：Ghrelin：是一种含有28个氨基酸残基的短肽，于1999年被发现，主要由胃底分泌，在下丘脑中也有表达，其可促进摄食、减少能量消耗和增加体质量，是目前发现的唯一促食欲激素。 Nesfatin-1：是一种由82个氨基酸组成的神经肽，于2006年被发现，具有减少摄食、调节能量平衡和减轻体质量的作用。 背景：均衡饮食和科学运动是公认的安全、有效且经济的体质量管理干预方式，但运动本身有时却提升了减肥者食欲，如果将低氧环境刺激和有氧运动干预结合，可能会收到最好的减质量效果。下丘脑作为机体调控摄食和能量平衡的中枢，其调控因子与肥胖症发病机制之间的关系备受关注。 目的：观察低氧或/和运动后肥胖大鼠下丘脑nesfatin-1和ghrelin水平变化，探讨低氧或/和运动影响机体摄食和体质量的神经内分泌机制。 方法：60只营养性肥胖SD大鼠均分为常氧安静组、常氧运动组、16.3%低氧安静组、16.3%低氧运动组、13.3%低氧安静组和13.3%低氧运动组，进行8周的低氧或/和运动干预。低氧环境采用低氧发生器分别营造体积分数为16.3%氧气和13.3%氧气环境，低氧干预组大鼠每天12 h在低氧环境中生活和运动；运动干预采用跑台运动方案(跑速20 m/min、坡度0°)，持续时间40 min，5 d/周。记录干预期大鼠体质量、摄食量，计算干预前后Lee’s指数，用ELISA试剂盒检测干预后大鼠下丘脑nesfatin-1和ghrelin水平。 结果与结论：①干预后大鼠体质量与Lee’s指数：单纯低氧环境刺激对大鼠体质量、Lee’s指数的影响没有单纯有氧运动刺激明显，而当低氧和运动结合时，其效果优于单一刺激；②干预期间大鼠日均摄食量：常氧安静组保持平稳，其余各组均减少，尤以16.3%低氧运动组、13.3%低氧运动组明显；③下丘脑nesfatin-1和ghrelin水平：低氧结合运动可影响大鼠下丘脑nesfatin-1水平，其中13.3%低氧运动组的nesfatin-1水平最高；单纯的运动或低氧均可影响大鼠下丘脑ghrelin水平，而单一运动刺激效果强于单一低氧刺激，当二者结合时降低效果更明显；④双因素方差分析：体质量和ghrelin水平受运动的影响，体质量、Lee’s指数和摄食量受氧气体积分数的影响，体质量、nesfatin-1和ghrelin水平受运动×氧气体积分数的影响；⑤结果表明，8周低氧运动可能通过影响肥胖大鼠下丘脑nesfatin-1与ghrelin水平来减少大鼠的摄食量，抑制其体质量增长，降低其Lee’s指数，但具体机制需待进一步研究。 ORCID: 0000-0002-1519-7825(范锦勤) 中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程     

Leptin responsiveness in mice that ectopically express agouti protein

Agouti protein is an endogenous antagonist of melanocortin receptors (MCR), including MCR3 and MCR4, which have been implicated as part of the hypothalamic mechanism that mediates leptin-induced hypophagia. In this experiment we examined the effects of peripheral and central leptin administration in male and female beta-actin promoter (BAPa) mice that express agouti protein ectopically and have a phenotype that includes obesity and diabetes which is exaggerated in males compared with females. Intraperitoneal infusion of 10 microg leptin/day for 13 days caused weight loss and a transient inhibition of food intake in wild-type mice, with a greater effect in males than females. Male BAPa mice were resistant to leptin infusion whereas female mice lost weight. All of the mice lost body weight following a single intracerebroventricular injection of leptin but the effect was greater in female BAPa mice than any other group. There also was a delayed suppression of food intake that was the same for wild-type and BAPa female mice, whereas food intake recovered faster in BAPa than wild-type males. The dissociation between food intake and body weight loss implies a significant effect of leptin on energy expenditure in BAPa mice. These results demonstrate that the effect of leptin on energy balance is not entirely dependent upon the melanocortin system.     

Effect of naltrexone on food intake and body weight in Syrian hamsters depends on metabolic status

Opioids are a family of neuropeptides involved in the control of food intake and regulation of body weight. In general, nonselective opioid antagonists have inhibited food intake in a variety of paradigms in rodent species. Syrian hamsters may be an exception to the general findings. In a previous report, we showed that systemic administration of an opioid antagonist, naltrexone, for 2 days increased body weight in female Syrian hamsters. To confirm the extent of these finding we designed the present experiment testing the effect of a chronic 6-day infusion of naltrexone on food intake, water intake, and body weight in freely feeding male hamsters. In addition, we examined the effect of acute administration of naltrexone on food intake in both ad-libitum-fed and food-deprived hamsters. We found that chronic systemic administration of naltrexone caused a significant increase in food intake and body weight. Second, acute administration of naltrexone decreased food intake after a 48-h fast but had no effect in ad-libitum-fed hamsters. Water consumption was not altered in any experimental paradigm. Our results suggest that opioid circuits in Syrian hamsters may function tonically to suppress food intake and body weight when Syrian hamsters are in positive energy balance. Paradoxically, opioids may enhance food intake after a sustained fast.     

Intermittent feeding and fasting reduces diabetes incidence in BB rats.

Food intake may be one of several factors which influence the risk of development of insulin dependent diabetes mellitus, but the influence of the pattern of food supply has not been studied previously. The aim of the present study was to investigate the effect of intermittent feeding and fasting upon diabetes in BB rats. This study included three groups. Group 1 served as control and included 77 animals, 79% became diabetic. In groups 2 and 3, after weaning, food but not water was withdrawn from the animals: 24 h twice a week in group 2; 24 h every second day in group 3. Group 2 included 40 BB rats, 50% (p < 0.004) became diabetic. Group 3 included 44 BB rats, 52% (p < 0.01) became diabetic. No differences were seen between sexes. Degree of insulitis was not influenced by changed food supply. Regarding blood glucose, no influence was seen among diabetic animals, among non-diabetic animals changed food supply reduced blood glucose values obtained at the end of the study. Intermittent feeding and fasting tended to reduce mean age at the time of diagnosis of diabetes, significance was reached only in female animals from group 3 compared to group 1. Body weight was obtained weekly. Intermittent feeding and fasting caused a reduced weight gain in group 2 as well as in group 3 compared to control animals; however, most pronounced in group 3 and also more pronounced among males compared to females. For pre-diabetic and non-diabetic animals comparable influence on body weight was seen. The main conclusion in the study is that intermittent feeding and fasting reduced diabetes incidence in BB rats.     

Behavioral thermoregulation in mice inoculated with influenza virus.

Mice housed at 30 degrees C and inoculated with a mouse-adapted influenza virus show a fall in body temperature (Tb) and a decrease in food intake to almost 0 grams per day. This study tested whether the fall in Tb could be accounted for by the decreased food intake and whether the fall in Tb was due to a decrease of thermoregulatory set point or to an inability to maintain Tb at set point level. The fall in Tb of influenza-infected mice was greater than that of food-deprived mice. When food deprived, mice given access to a thermal gradient increased their preference for warmer areas in the gradient and, as a result, Tb did not fall as much as Tb of starved mice not given access to a thermal gradient. When infected with influenza virus, mice given a thermal gradient decreased Tb less and at a slower rate than mice not given a gradient. However, this fall in Tb of influenza-infected mice was greater than that of food-deprived mice given a thermal gradient. Mice given a thermal gradient increased their preference for the warmer temperatures after inoculation; this returned to preinoculation preference for cooler temperatures during the later days of infection despite a continuous fall in Tb. Influenza-infected mice given a thermal gradient survived significantly fewer days than infected mice not given a thermal gradient. We conclude that the influenza-induced fall of Tb in mice cannot be explained solely by the decrease in food intake, and is partially due to a decrease in thermoregulatory set point.     

Food habits and nutritional status assessment of adolescent soccer players. A necessary and accurate approach.

The aim of this study was to assess the food habits and nutritional status of high level adolescent soccer players (N = 33; ages 14-16 yrs) living in their home environment. Body composition (height, mass, skinfolds), biochemical and hematological parameters, performance in soccer-specific tests (sprinting, jumping, intermittent endurance), and dietary intake (weighed food intake method) and related behaviors (nutrient supplement use, daily activity profile) were assessed. Daily energy expenditure and energy intake were 12.5 MJ and 12.6 MJ, respectively. Protein (16% of energy intake; 1.9 g/kg of body mass), lipid (38%), and cholesterol (385 mg) intake were above recommendations, while carbohydrates (45%) were below. The food intake of these adolescents was based on cereals and derivates; meat, fish, and eggs; milk and dairy products; biscuits and confectionery; and oil, butter and margarine, which provided 78% of total energy intake, 85% of proteins, 64% of carbohydrates, 90% of lipids, and 47% of fiber. Although diet provided sufficient iron, 48% of individuals showed iron deficiency without anemia. Based on these results, a well designed nutrition intervention would be advisable for optimizing performance, and especially for promoting healthy eating habits in adolescent soccer players.     

Urine C-peptide excretion in hypocaloric states and factors affecting its excretion]

Recent evidence suggests that hyperinsulinemia may contribute to the development of various risk factors of atherosclerosis. To examine the effects of energy intake on insulin secretion, 24-h urine C-peptide was measured in twelve women with rheumatoid arthritis who were not taking any medicine and stayed in Koda hospital for a diet therapy which lasted 55 days. They were basically placed on a 1200 kcal/day vegan diet combined with three 3-5-day fasting periods (200 kcal/day). Urine C-peptide excretion markedly decreased from 31-40 to 8-14 micrograms/day during the fasting periods. Among the anthropometric variables examined, the average level of urine C-peptide excretions measured in the fasting periods showed a significant correlation with the percentage and the amount of body fat. However, such correlation was not observed while the calorie intake was 1200 kcal. No clinical laboratory parameter showed a significant correlation with urinary C-peptide excretion. These results suggest that the major determinant of urine C-peptide excretion is food intake and that hyperinsulinemia could be easily improved by restricting energy intake.     

Food intake before migraine attacks in children

A questionnaire survey of 120 children with migraine showed an average age of onset of 5·15 years, an equal sex ratio under nine years, and a positive family history in 79 per cent. Eye symptoms (42 per cent) and headaches (32 per cent) heralded an attack, with abdominal pain and vomiting later and less frequent. Visual aura was not recognized under five years, but occurred in 52 per cent of the 13 to 15 year age group. Most attacks occurred on schooldays and 82 per cent were over within two days.

The 24-hour food intake before an attack was compared with the food intake seven days later when no migraine occurred. This suggested that fasting (41 per cent) or specific foods (38 per cent) could have been responsible for many of the attacks.

     

A role of the histaminergic system for the control of feeding by orexigenic peptides

A considerable number of neuropeptides are involved in the hypothalamic regulation of feeding behavior. We previously reported that leptin, the ob gene product, expressed its anorectic effect though the histaminergic system via histamine H(1) receptors. However, the interactions among the orexigenic neuropeptides, such as orexin-A, neuropeptide Y (NPY), and ghrelin, and the histaminergic system have not yet been clarified. In this study, we investigated the effect of the neuropeptides on the hypothalamic histamine release in rats, and on food intake and locomotor activity in H(1)-receptor knockout (H1R-KO) mice. Orexin-A increased the histamine release and locomotor activity, but not food intake, suggesting that the histaminergic system participates in arousal rather than feeding by orexin-A. NPY also increased histamine release, but its effect was not immediate. NPY-injected H1R-KO mice consumed more food than the wild-type mice; thus, the histaminergic system may act as a feedback factor downstream of NPY. Ghrelin did not affect histamine release, and it increased food intake, even in H1R-KO mice. Thus, ghrelin expresses its action in a histamine-independent manner.     

Anti-diabetic effect of ginsenoside Rb(3) in alloxan-induced diabetic mice

As one of the main active component of protopanaxdiol type ginsenosides, ginsenoside Rb(3) is rarely reported in the treatment of diabetes. The anti-diabetic activity of ginsenoside Rb(3) was investigated in a model of alloxan-induced diabetic mice in the present study. The physiological parameter such as fasting blood glucose level, oral glucose tolerance, body weight, food intake and water intake were measured. Glucose consumption in C2C12 myotubes was also determined in order to investigate the molecular mechanism of ginsenoside Rb(3) in anti-diabetes. The alloxan-induced diabetic mice were treated with ginsenoside Rb(3) for 2 weeks at doses of 5 mg/kg, 15 mg/kg and 25 mg/kg. After 2 weeks treatment of ginsenoside Rb(3), the fasting blood glucose levels of DG 15 and DG 25 were respectively reduced by 36.70% and 37.50% compared to control group. At a dose of 25 mg/kg, oral glucose tolerance was significantly improved compared to control group (P < 0.05). The AUC decreased by 34.47% (from 2442 ± 291 mmol·min/L to 1600 ± 109 mmol·min/L). Both food intake and water intake were remarkably lowered. The injury of pancreas tissues was repaired, which was observed by using HE staining and optic microscope. In vitro, at concentrations of 100 and 200 μM, ginsenoside Rb(3) increased glucose consumption in C2C12 myotubes by 76.83% and 97.20%, respectively, as compared to the control group. However, the body weight of diabetic mice was not significantly altered. In conclusion, our results showed that ginsenoside Rb(3) reduced fasting blood glucose level, food intake, water intake, improved oral glucose tolerance, and repaired injured pancreas tissues of alloxan-induced diabetic mice. Therefore, it was suggested that ginsenoside possesses the potential of the clinical use in preventing and treating diabetes.     

Effect of starvation or restriction on self-selection of macronutrients in rats.

Two models of food deprivation were used to study feeding behavior: starvation and dietary restriction. Rats starved for 3 days had decreased protein intake during the first 2 days of refeeding followed by increased carbohydrate consumption compared to controls. During refeeding, total intake was initially low compared to controls. In a second starvation study of similar design, brain tissues [raphe, ventromedial hypothalamus (VMH)] and sera were collected for analysis before refeeding and on day 2 of refeeding. Starved and starved-refed rats had increased serum beta-hydroxybutyrate versus controls. In rats restricted for 5 days (5 g/day), total food intake was increased immediately and was characterized primarily by carbohydrate intake. Serotonin levels in the raphe were decreased in restricted rats and 5-hydroxyindole acetic acid (5-HIAA) increased in restricted-refed rats. Restriction caused an increase in blood levels of beta-hydroxybutyrate and a decrease in insulin and glucose compared to controls. Fat selection remained low throughout all studies. The data suggest that starvation and food restriction elicit different patterns of macronutrient selection upon refeeding.     

A sex difference in the response to fasting

We determined whether women and men would alter their pattern of food intake after they had deprived themselves of food. We found that women consumed 12% less food after fasting and that men ate 28% more food after fasting. Serving more food on the test day did not increase food intake of women. Women, who ate at a nearly constant rate (linear eaters), consumed less food than those eating at an initially high speed which decreased over the course of the meal (decelerated eaters). Women decreased their food intake after fasting as their eating pattern became more linear. After fasting, men increased their food intake, and the rate at which they ate became more decelerated. Food intake of both women and men was normalized after fasting by providing feedback that encouraged them to eat according to the pattern they showed in the non-fasted condition. The results support the hypothesis that linear eating, and the dieting that elicits linear eating, are risk factors for the development of the abnormal linear eating pattern that characterizes patients with anorexia nervosa. The data also provide additional support for the use of behavioral feedback to normalize the pattern of eating for individuals who have difficulty maintaining their body weight.     

Intermittent Fasting Promotes Bacterial Clearance and Intestinal IgA Production in Salmonella typhimurium‐Infected Mice

The impact of intermittent fasting versus ad libitum feeding during Salmonella typhimurium infection was evaluated in terms of duodenum IgA levels, bacterial clearance and intestinal and extra‐intestinal infection susceptibility. Mice that were intermittently fasted for 12   weeks or fed ad libitum were infected with S. typhimurium and assessed at 7 and 14 days post‐infection. Next, we evaluated bacterial load in the faeces, Peyer's patches, spleen and liver by plate counting, as well as total and specific intestinal IgA and plasmatic corticosterone levels (by immunoenzymatic assay) and lamina propria IgA levels in plasma cells (by cytofluorometry). Polymeric immunoglobulin receptor, α‐ and J‐chains, Pax‐5 factor, pro‐inflammatory cytokine (tumour necrosis factor‐α and interferon‐γ) and anti‐inflammatory cytokine (transforming growth factor‐β) mRNA levels were assessed in mucosal and liver samples (by real‐time PCR). Compared with the infected ad libitum mice, the intermittently fasted infected animals had (1) lower intestinal and systemic bacterial loads; (2) higher SIgA and IgA plasma cell levels; (3) higher mRNA expression of most intestinal parameters; and (4) increased or decreased corticosterone levels on day 7 and 14 post‐infection, respectively. No contribution of liver IgA was observed at the intestinal level. Apparently, the changes following metabolic stress induced by intermittent fasting during food deprivation days increased the resistance to S. typhimurium infection by triggering intestinal IgA production and presumably, pathogen elimination by phagocytic inflammatory cells.