Reduced caloric intake and periodic fasting independently contribute to metabolic effects of caloric restriction

Caloric restriction (CR) has positive effects on health and longevity. CR in mammals implements time‐restricted (TR) feeding, a short period of feeding followed by prolonged fasting. Periodic fasting, in the form of TR or mealtime, improves metabolism without reduction in caloric intake. In order to understand the relative contribution of reduced food intake and periodic fasting to the health benefits of CR, we compared physiological and metabolic changes induced by CR and TR (without reduced food intake) in mice. CR significantly reduced blood glucose and insulin around the clock, improved glucose tolerance, and increased insulin sensitivity (IS). TR reduced blood insulin and increased insulin sensitivity, but in contrast to CR, TR did not improve glucose homeostasis. Liver expression of circadian clock genes was affected by both diets while the mRNA expression of glucose metabolism genes was significantly induced by CR, and not by TR, which is in agreement with the minor effect of TR on glucose metabolism. Thus, periodic fasting contributes to some metabolic benefits of CR, but TR is metabolically different from CR. This difference might contribute to differential effects of CR and TR on longevity.     

A new light on caloric test--what was disclosed by three dimensional analysis of caloric nystagmus?

For better understanding of caloric nystagmus, this phenomenon will be reviewed historically in three stages. 1) The first light on caloric nystagmus was thrown by Barany 1906. Through direct observation of eye movements, Barany established the caloric test as an important tool to determine the side of lesion for vertigo. 2) The second light is shed by electrooculogram (EOG) from the late 1950th. EOG enabled qualitative analysis of caloric nystagmus, and proved Barany's convection theory, but resulted in neglect of vertical and roll eye movements. 3) The third light is gained by 3D recording of eye movements started from the late 1980th. 3D recordings of eye movements enabled us to analyze the spatial orientation of caloric nystagmus, and disclose the close correlation of the nystagmus components in the head vertical and the space vertical planes, suggesting a contribution of the velocity storage integrator. The 3D property of caloric nystagmus will be explained in detail.     

Effect of caloric restriction on depression

Recently, most of evidence shows that caloric restriction could induce antidepressant‐like effects in animal model of depression. Based on studies of the brain–gut axis, some signal pathways were common between the control of caloric restriction and depression. However, the specific mechanism of the antidepressant‐like effects induced by caloric restriction remains unclear. Therefore, in this article, we summarized clinical and experimental studies of caloric restriction on depression. This review may provide a new therapeutic strategy for depression.     

植物热值及其生物生态学属性

介绍了热值的定义、表示方法、研究意义和植物热值在生态学中的研究历史与现状;分析了植物热值的时空变异性,包括热值在种间和类群间的变异及热值的种内变异规律;探讨了影响植物热值变化的因子(包括气候、立地条件、胁迫环境和人为干扰等)和热值变异的内在决定因素(包括碳浓度、灰分含量及有机质化学组成等);对植物热值的研究前景和局限性进行了展望。     

Transcriptomics applied to obesity and caloric restriction

Caloric restriction still remains the most efficient way to promote weight loss. Deciphering the molecular basis of adaptation to energy restriction is critical for the tailoring of new therapeutic strategies. This review focuses on the recent input of gene profiling on adipose tissue in obesity pathogenesis and on the new insights on adaptations occurring during very low caloric diet (VLCD) in humans. Hypocaloric diets improve a wide range of metabolic parameters including lipolytic efficiency, insulin sensitivity, and inflammatory profile. In the subcutaneous white adipose tissue (scWAT) the VLCD induced a decrease in the mRNA levels for the antilipolytic alpha2-adrenergic receptor associated with changes in catecholamine-induced adipocyte lipolytic capacity. The improvement in insulin sensitivity was not associated with a change in subcutaneous adipose tissue adiponectin gene expression or in its plasma level, suggesting that adiponectin is not involved in the regulation of VLCD-induced improvement of insulin sensitivity and that there is a small contribution of subcutaneous adipose tissue to plasma adiponectin levels. Pangenomic microarray studies in human scWAT revealed that a panel of inflammatory markers and acute phase reactants were over expressed in obese compared to lean subjects. Caloric restriction improved the inflammatory profile of obese subjects through a decrease of pro-inflammatory factors and an increase of anti-inflammatory molecules. These genes were mostly expressed in the stroma vascular fraction of the adipose tissue. Specific cell-type isolation and immunohistochemistry demonstrated that monocyte/macrophage lineage cells were responsible for the expression of both mRNA and protein inflammatory markers. The acute phase proteins serum amyloid A was highly expressed in mature adipocytes from obese subjects. Caloric restriction decreased both serum amyloid mRNA and circulating levels. Obesity now clearly appears as chronic low-grade inflammation state. Modulation of the inflammatory pathways may represent new therapeutic targets for the treatment of obesity-related complications.     

The hyperleptinemia of obesity-regulator of caloric surpluses

New evidence suggests that leptin and other anorexigenic agents reduce appetite by inactivating hypothalamic AMP-activated protein kinase (AMPK), thereby increasing malonyl CoA levels. This preview examines AMP biology and its role in malonyl-CoA generation and attempts to integrate its central actions with its peripheral antilipotoxic actions within the context of leptin physiology in obesity.     

Enhancement of mitochondrial function correlates with the extension of lifespan by caloric restriction and caloric restriction mimetics in yeast

Caloric restriction mimetics (CRMs) have been developed to mimic the effects of caloric restriction (CR). However, research reports for the effects of CRMs are often times inconsistent across different research groups. Therefore, in this study, we compared seven identified CRMs which extend the lifespans of various organisms including caffeine, curcumin, dapsone, metformin, rapamycin, resveratrol, and spermidine to CR for mitochondrial function in a single model, Saccharomyces cerevisiae. In this organism, rapamycin extended chronological lifespan (CLS), but other CRMs failed to extend CLS. Rapamycin enhanced mitochondrial function like CR did, but other CRMs did not. Both CR and rapamycin worked on mitochondrial function, but they worked at different windows of time during the chronological aging process.     

Seasonal variations of caloric values in herbaceous plants

Summary In 1975 some higher herbaceous plants of two different habitats were investigated according to seasonal variations of their caloric values both on a dry weight base and on an ash-free dry weight base. In eight speceis of a meadow and an old-field community, which were harvested each second month from February to December 1975, there were slight changes in energy content despite the fact that only flowering stages have been analysed. The reasons for these variations are climatic resp. endogenous ones.     

Orexin A-induced feeding is augmented by caloric challenge

Orexin neurons are stimulated by conditions that are glucoprivic, suggesting that orexin signaling may be increased during nutritional duress. We have previously shown that injection of orexin A (OxA) into the rostral lateral hypothalamic area (rLHa) robustly and dose-dependently increases feeding behavior. Thus we hypothesized that exogenous administration of orexin A would induce a greater feeding response after acute food deprivation or perceived caloric duress achieved through 2-deoxyglucose (2DG) administration. To test our hypothesis, male Sprague-Dawley rats implanted with internal guide cannulas directed to the rLHa were exposed to varying degrees of food deprivation (0, 3, 12, 24 h) and 2DG (200 mg/kg) before intra-rLHa OxA (500 pmol) infusion. We also performed a dose-response study using graded doses of OxA (0, 31.25, 125, and 500 pmol) in fed and 24-h fasted rats. OxA administration in conjunction with the highest level of prior food deprivation (24 h) resulted in the greatest feeding response (above baseline means; 0 h deprivation: 1.9 +/- 0.6; 24 h deprivation: 4.4 +/- 0.8; P = 0.0034) and showed a dose-dependent enhancement of feeding. Additionally, 2DG administration before OxA administration resulted in a significantly higher feeding response (above baseline means: 2DG = 1.8 +/- 0.5; OxA = 1.8 +/- 0.4; 2DG + OxA = 5.1 +/- 0.6; P < 0.0001). These data support the hypothesis that orexin signaling may be important in modulating the feeding network under times of nutritional duress.     

热量限制与白藜芦醇抗衰老的研究进展

限制热量摄取(caloric restriction,CR) 能够延长寿命,这个75 年前的发现己得到广泛的证明.其作用主要是由去乙酰化酶 (Sir2/SIRT1)所介导.近年又发现,植物中的多酚化物--白藜芦醇,是SIRT1 的激活剂,它能够模拟 CR 的抗衰老作用,并能防治多种疾病.因此它有可能成为人类防病和抗衰老的有用工具.     

Imperfect information on physical activity and caloric intake

Using the National Health and Nutrition Examination Survey Data, I find that individuals who overestimate their activity level by one standard deviation consume 40–60 extra calories per day, or enough to gain five pounds per year. These extra calories are composed mainly of sugar and carbohydrate, and are concentrated among individuals in the 75th and 90th percentiles of caloric intake. The link between overeating and inaccurate estimation of physical activity is strongest among less educated individuals and individuals with high variance in their physical activity, suggesting that imperfect recall or information gaps explain at least part of the relationship of interest. These results imply the existence of a necessary condition for physical activity-based information treatments to be effective in changing health behaviors and obesity rates.     

The impact of weight stigma on caloric consumption

The present study assessed the influence of exposure to weight stigma on energy intake in both overweight and normal-weight adult women. Seventy-three women (mean age: 31.71 ± 12.72 years), both overweight (n = 34) and normal weight (n = 39), were randomly assigned to view one of two videos depicting either weight stigmatizing material or neutral material, after which they consumed snacks ad libitum. Pre- and post-video measures included blood pressure, attitudes toward overweight individuals, and positive and negative affect. Participants' body weight was measured, as was the number of kilocalories consumed following video exposure. Overweight women who watched the stigmatizing video ate more than three times as many kilocalories as overweight women who watched the neutral video (302.82 vs. 89.00 kcal), and significantly more calories than the normal-weight individuals who watched either the stigmatizing or the neutral video. A two-by-two analysis of covariance revealed that even after adjusting for relevant covariates, there was a significant interaction between video type and weight status in that when overweight, individuals consumed significantly more calories if they were in the stigmatizing condition vs. the neutral condition (F(1,65) = 4.37, P = 0.04, η(2) = 0.03). These findings suggest that among overweight women, exposure to weight stigmatizing material may lead to increased caloric consumption. This directly challenges the notion that pressure to lose weight in the form of weight stigma will have a positive, motivating effect on overweight individuals.     

Role of sleep timing in caloric intake and BMI

Sleep duration has been linked to obesity and there is also an emerging literature in animals demonstrating a relationship between the timing of feeding and weight regulation. However, there is a paucity of research evaluating timing of sleep and feeding on weight regulation in humans. The goal of this study was to evaluate the role of sleep timing in dietary patterns and BMI. Participants included 52 (25 females) volunteers who completed 7 days of wrist actigraphy and food logs. Fifty-six percent were "normal sleepers" (midpoint of <5:30 AM) and 44% were "late sleepers" (midpoint of sleep ≥5:30 AM). Late sleepers had shorter sleep duration, later sleep onset and sleep offset and meal times. Late sleepers consumed more calories at dinner and after 8:00 PM, had higher fast food, full-calorie soda and lower fruit and vegetable consumption. Higher BMI was associated with shorter sleep duration, later sleep timing, caloric consumption after 8:00 PM, and fast food meals. In multivariate models, sleep timing was independently associated with calories consumed after 8:00 PM and fruit and vegetable consumption but did not predict BMI after controlling for sleep duration. Calories consumed after 8:00 PM predicted BMI after controlling for sleep timing and duration. These findings indicate that caloric intake after 8:00 PM may increase the risk of obesity, independent of sleep timing and duration. Future studies should investigate the biological and social mechanisms linking timing of sleep and feeding in order to develop novel time-based interventions for weight management.