Thesis (M.A.)--Columbia Biblical Seminary and Graduate School of Missions, Columbia, S.C., 1994. / Abstract. Includes bibliographical references (leaves 124-125, 128-137).

No description available.

Hypohydration and fasting are used as means to achieve body mass loss and Ramadan fasting is practised by millions of Muslims as a religious custom. Although both hypohydration and fasting have been studied extensively, the effect of hypohydration and Ramadan style fasting on many aspects of human performance is still unclear. In Chapter 3, the effect of exercise-induced hypohydration on muscle performance was evaluated. The protocol was developed to eliminate masking and exacerbating factors such as changes in muscle glycogen storage, muscle temperature, fatigue and fluid distribution change and acid base status. Muscle strength and endurance decreased due to hypohydration equivalent to 2% of body mass. This suggests that hydration status itself can affect adversely athletes' performance. In Chapter 4, the effect of one day (11 h) of Ramadan style fasting on some aspects of exercise performance during the day was investigated. Participants were tested three times throughout the day: at 7:00 am, 12:00 noon and 7:00 pm. 11 h of Ramadan style fasting decreased body mass by 2.1%. No change was found in exercise performance measurements. The results of this study suggest that this short period of fasting has no measurable effects on performance and/or that any effects are compensated by the circadian rhythm throughout the day. However, most athletes use more intense fasting or several consecutive days of fasting to achieve their weight reduction goal. In Chapter 5, the effect of Ramadan fasting (one month long intermittent fasting) on some aspects of exercise performance of athletes (weight category and non-weight category sports) and recreationally active individuals was studied. Participants were tested before, during (after the first week and in the last week) and after the month of Ramadan. Ramadan style living (involving a change in timing of food intake and sleep pattern) affects most of the anthropometric and physical performance parameters of the athletes and of the recreationally active subjects, with no difference in the pattern of change between groups. Almost all of the differences were recovered a week after the end of fasting. Chapter 6 contains the results of three studies focused on the effects of fasting on cognitive function (study A- breakfast elimination; study B- one day (11 h) of Ramadan style fasting; and study C- one month of Ramadan fasting). Results of these studies make a logical conclusion that fasting has a detrimental effect on memory, reaction time and accuracy of responses. The pattern of the effects showed differences that may be related to various participants' characteristics (age group, gender) and the nature of intervention. In summary, Ramadan style fasting may affect performance of some mental and physical tasks in some, but perhaps not in all individuals.

Background: The increased incidence of obesity and associated metabolic diseases has driven research focused on genetically or pharmacologically alleviating metabolic dysfunction. These studies employ a range of fasting-refeeding models including 4-24 h fasts, "overnight" fasts, or meal feeding. Still, we lack literature that describes the physiologically relevant adaptations that accompany changes in the duration of fasting and re-feeding. Since the liver is central to whole body metabolic homeostasis, we investigated the timing of the fast-induced shift toward glycogenolysis, gluconeogenesis, and ketogenesis and the meal-induced switch toward glycogenesis and away from ketogenesis. Methods: Twelve to fourteen week old male C57BL/6J mice were fasted for 0, 4, 8, 12, or 16 h and sacrificed 4 h after lights on. In a second study, designed to understand the response to a meal, we gave fasted mice access to feed for 1 or 2 h before sacrifice. We analyzed the data using mixed model analysis of variance. Results: Fasting initiated robust metabolic shifts, evidenced by changes in serum glucose, non-esterified fatty acids (NEFAs), triacylglycerol, and beta-OH butyrate, as well as, liver triacylglycerol, non-esterified fatty acid, and glycogen content. Glycogenolysis is the primary source to maintain serum glucose during the first 8 h of fasting, while de novo gluconeogenesis is the primary source thereafter. The increase in serum a-OH butyrate results from increased enzymatic capacity for fatty acid flux through beta-oxidation and shunting of acetyl-CoA toward ketone body synthesis (increased CPT1 (Carnitine Palmitoyltransferase 1) and HMGCS2 (3-Hydroxy-3-Methylglutaryl-CoA Synthase 2) expression, respectively). In opposition to the relatively slow metabolic adaptation to fasting, feeding of a meal results in rapid metabolic changes including full depression of serum a-OH butyrate and NEFAs within an hour. Conclusions: Herein, we provide a detailed description of timing of the metabolic adaptations in response to fasting and re-feeding to inform study design in experiments of metabolic homeostasis. Since fasting and obesity are both characterized by elevated adipose tissue lipolysis, hepatic lipid accumulation, ketogenesis, and gluconeogenesis, understanding the drivers behind the metabolic shift from the fasted to the fed state may provide targets to limit aberrant gluconeogenesis and ketogenesis in obesity.

This project aimed to investigate the role of the γ-lactone of 3,4-dihydroxybutanoic acid (3,4DB) which was claimed by Japanese investigators to be one of several endogenous γ-lactones involved in the control of food intake. Tissue, plasma and urine organic acid profiles were screened for the γ-lactone of 3,4DB using both GC and GCMS. Careful mass spectral analysis and <I>in vitro</I> acid-γ-lactone exchange analyses with structural validation studies showed that the γ-lactone of 3,4DB did not occur <I>in vivo</I> but that the free acid of 3,4DB did. This rejects previous claims to the contrary. Fasting increased rat plasma 3,4DB with urinary output significantly elevated for the first 24h of fasting. A metabolic route from glutamate to acetate is proposed with 3,4DB as an intermediate. Peripheral administration of glutamate, γ-aminobutyric acid (GABA) and 4-hydroxybutyric acid (4HB) to rats reduced food intake with increasing effects at each stage of the pathway. The γ-lactone 2-buten-4-olide is toxic and other γ-lactones had more potent effects than their free acids on rats. The intragastric administration of GABA stimulated 4HB production <I>in vivo</I> and GABA or 4HB increased plasma 3,4DB levels, thus implying that 3,4DB occurs at an intermediate in our proposed pathway. A likely endogenous source of 3,4DB is as a minor GABA metabolite. The response of the free acid of 3,4DB to fasting followed a similar trend as that reported for its γ-lactone and related γ-lactones are unlikely to occur <I>in vivo</I>. Given the similarities of 4HB (a precursor of 3,4DB) and 3,4DB in structure to the ketone body 3-hydroxybutyrate (3HB) and the similarity of 3,4DB in fasting response to 3HB, both 4HB and 3,4DB may initiate anorexia in fasting.

Graduation date: 1993

Thesis (D. Min.)--Westminster Theological Seminary, Philadelphia, 1989. / Text in English and Spanish. Spanish title of manual: Manual para el ministerio de la oración. Includes bibliographical references (leaves 230-246).

The purpose of this study was to determine reserves of riboflavin in urine of college women.

The coronavirus disease 2019 (COVID-19) pandemic is provoking a global public health crisis. Even though the academic world is intensively pursuing new therapies, there is still no “game changer” in the management of COVID 19. The Mammalian Target of Rapamycin (mTOR) is an ancient signaling system that has been proposed as a molecular tool used by coronaviruses and other RNA and DNA viruses in order to replicate and persist in the host cell. In recent years, Intermittent Fasting (IF), a practice consisting on a strict calorie restriction during a prolonged period of time during the day, has gained popularity due to its potential benefits in multiple health systems and in regulating inflammation. IF inhibits the mTOR pathway which is similar to the effects of Rapamycin in some animal models. mTOR inhibition and promotion of autophagy could potentially be the link between the possible direct benefits of IF in COVID-19 due to the interruption of the viral cycle (protein synthesis). Besides, IF has shown to be a strong anti-inflammatory in multiple prior studies, and may play a role in attenuating COVID -19 severity. This review hypothesizes the possible intersection between viral, immunological, and metabolic pathways related to mTOR and the potential mechanisms through which IF may improve clinical outcomes. Future prospective randomized controlled clinical trials to evaluate intermittent fasting (IF) regimens in order to prevent and treat moderate to severe forms of COVID-19 in humans are needed. / Revisión por pares

The developing brain is highly sensitive to environmental influences. Unfavorable nutrition is one kind of stress that can cause acute metabolic disorders during the neonatal period [1,2,3] and severe diseases in later life [4,5]. These early life experiences occurring during heightened periods of brain plasticity help determine the lifelong structural and functional aspects of brain and behavior. In humans, for example, weight gain during the first week of life increased the propensity for developing obesity several decades later [5]. This susceptibility is, if not all, related to the dynamic reversible epigenetic imprints left on the histones [6,7,8], especially during the prenatal and postpartum period [9]. Histones are highly dynamic and responsive towards environmental stress [10,11]. Through covalent modification of the histone tail, histones are able to direct DNA scaffolding and regulate gene expression [10,12]. Thus far, various types of post translational modifications have been identified on various histones tails [12]. Among them, the methylation and acetylation on lysine residue (K) 27 on histone 3 (H3) has been tightly linked to gene repression [13,14] and activation [15], respectively. EZh2 (enhancer of zeste 2) in the polycomb repressive complex 2 (PRC2) is the only methyltransferase that has been linked to catalyze this methylation reaction. In addition, SUZ (suppressor of zeste) and EED (embryonic ectoderm development) are two other key proteins in PRC2 function core that help EZH2. As previous reported, increased H3K27 methylation was monitored after fasting stress during neonatal period in chicks' paraventricular nucleus (PVN). In this study, we investigated the detailed mechanism behind changes in H3K27 methylation following fasting stress. After 24 hours fasting on 3 days-of-age (D3), chicks exhibited elevated mRNA levels of PRC2 key components, including EZH2, SUZ and EED, in the PVN on D4. Western blots confirmed this finding by showing increased global methylation status at the H3K27 site in the PVN on D4. In addition, until 38 days post fasting, SUZ and EZH2 remained inhibited. A newly identified anorexigenic factor, Brain-derived neurotrophic factor (BDNF), was used as an example of multiple hormones expressed in PVN to verify this finding. Both BDNF protein and mRNA exhibited compatible changes to global changes of tri- (me3) and di-methylated (me2) H327. Furthermore, by using chromatin immunoprecipitation assays (ChIP), we were able to monitor the changes of H3K27me2/me3 deposition along the Bdnf gene. Fasting significantly increased H3K27me2/me3 as well as EZH2 at the Bdnf's promoter, transcription start site and 3'-untranslated region. These data show that fasting stress during the early life period could leave epigenetic imprinting in PVN for a long time. Next, we tried to understand the function of this epigenetic imprinting in the chicks' PVN. Thus, we compared naive chicks (never fasted) to chicks that received either a single 24 hour fast on D3 or two 24 hour fast on both D3 and 10 days-of-age (D10). We found that the D3 fasted group significantly increased the level of PRC2 key components and its product H3K27me2/me3 compared to the naive group. However, D3 fasting and D10 fasting together decreased the surges of H3K27me2/me3, SUZ and EED (not EZH2) compared to the naive group. We called this phenomenon "epigenetic memory". The Western blot, qPCR and CHIP assay results from BDNF all confirmed the existence of "epigenetic memory" for PRC2. These data suggested that fasting stress during the early period of brain development could leave long term epigenetic modifications in neurons. These changes could be beneficial to the body, which keeps homeostasis of inner environment and prevent massive response to future same stress. The EZH2 protein was knocked down and the H3K27 methylation status changes were monitored after applying the same treatment. We first confirmed that EZH2 antisense oligonucleotides (5.5 ug), but not EZH2 siRNA and artificial cerebrospinal fluid (ACSF), inhibit EZH2 protein by 86 % in the PVN. Then, on D3, chicks were subjected to a 24 hour fasting stress (D3-fasting) post either EZH2 antisense or ACSF injection. The EZH2 antisense blocked the surge of both EZH2 mRNA and H3K27 methylation after D3-fasting. At the same time, BDNF exhibited elevated expression levels and less methylated H3K27 deposition along the Bdnf gene. In addition, we were also interested in the changes of "epigenetic memory" post EZH2 antisense injection. We found that after EZH2 antisense injection, chicks' PVN no longer exhibited any "epigenetic memory" to repetitive fasting stress. While EZH2 mRNA was constantly inhibited, SUZ, EED and H3K27me2/3 levels were unpredictable. These findings suggested that neurons in the PVN utilized PRC2 as a major H3K27 methylation tool. Knockdown of EZH2 in the PRC2 impaired the proper response in PVN to fasting stress and PVN's ability to acclimate to repetitive fasting stresses. Thus, EZH2 is an important H3K27 methyltransferase inside chicken hypothalamus to maintain homeostasis. In conclusion, fasting stress during the early life period could leave epigenetic markers on chromosomes of neurons in the feeding regulation center. These epigenetic markers will be left on chromosomes for a long period of time and have a beneficial role in keeping homeostasis when individuals face future fasting stress again. H3K27 methylation is one of these epigenetic markers and inhibits expression of various genes inside neurons. EZH2 is so far the only detected methyltransferases for H3K27 that form the PRC2. Thus EZH2 plays a key function in the body's response to fasting. / Ph. D.