scholarly journals When to eat? The influence of circadian rhythms on metabolic health: are animal studies providing the evidence?

2016 ◽  
Vol 29 (2) ◽  
pp. 180-193 ◽  
Author(s):  
Sofía Moran-Ramos ◽  
Adrian Baez-Ruiz ◽  
Ruud M. Buijs ◽  
Carolina Escobar
Keyword(s):  
Food Intake ◽  
Circadian Rhythms ◽  
Animal Studies ◽  
Metabolic Regulation ◽  
Metabolic Diseases ◽  
High Energy ◽  
The Body ◽  
Human Studies ◽  
Metabolic Disturbances ◽  
Behavioural Aspects

AbstractAs obesity and metabolic diseases rise, there is need to investigate physiological and behavioural aspects associated with their development. Circadian rhythms have a profound influence on metabolic processes, as they prepare the body to optimise energy use and storage. Moreover, food-related signals confer temporal order to organs involved in metabolic regulation. Therefore food intake should be synchronised with the suprachiasmatic nucleus (SCN) to elaborate efficient responses to environmental challenges. Human studies suggest that a loss of synchrony between mealtime and the SCN promotes obesity and metabolic disturbances. Animal research using different paradigms has been performed to characterise the effects of timing of food intake on metabolic profiles. Therefore the purpose of the present review is to critically examine the evidence of animal studies, to provide a state of the art on metabolic findings and to assess whether the paradigms used in rodent models give the evidence to support a ‘best time’ for food intake. First we analyse and compare the current findings of studies where mealtime has been shifted out of phase from the light–dark cycle. Then, we analyse studies restricting meal times to different moments within the active period. So far animal studies correlate well with human studies, demonstrating that restricting food intake to the active phase limits metabolic disturbances produced by high-energy diets and that eating during the inactive/sleep phase leads to a worse metabolic outcome. Based on the latter we discuss the missing elements and possible mechanisms leading to the metabolic consequences, as these are still lacking.

scholarly journals Meal Timing, Aging, and Metabolic Health

2019 ◽  
Vol 20 (8) ◽  
pp. 1911 ◽  
Author(s):  
Katharina Kessler ◽  
Olga Pivovarova-Ramich
Keyword(s):  
Circadian Rhythms ◽  
Circadian Clock ◽  
Dietary Patterns ◽  
Metabolic Regulation ◽  
Metabolic Diseases ◽  
Metabolic Health ◽  
Health Concern ◽  
Metabolic Disturbances ◽  
Beneficial Effects ◽  
Meal Timing

A growing body of evidence suggests that meal timing is an important factor for metabolic regulation and that the circadian clock tightly interacts with metabolic functions. The proper functioning of the circadian clock is critical for maintaining metabolic health. Therefore, chrononutrition, a novel discipline which investigates the relation between circadian rhythms, nutrition, and metabolism, has attracted increasing attention in recent years. Circadian rhythms are strongly affected by obesity, type 2 diabetes, and other dietary-induced metabolic diseases. With increasing age, the circadian system also undergoes significant changes which contribute to the dysregulation of metabolic rhythms. Metabolic diseases are a major health concern, particularly in light of a growing aging population, and effective approaches for their prevention and treatment are urgently needed. Recently, animal studies have impressively shown beneficial effects of several dietary patterns (e.g., caloric restriction or time-restricted feeding) on circadian rhythms and metabolic outcomes upon nutritional challenges. Whether these dietary patterns show the same beneficial effects in humans is, however, less well studied. As indicated by recent studies, dietary approaches might represent a promising, attractive, and easy-to-adapt strategy for the prevention and therapy of circadian and metabolic disturbances in humans of different age.

Roux-en-Y Gastrointestinal Bypass Promotes Activation of TGR5 and Peptide YY

2020 ◽  
Vol 20 (8) ◽  
pp. 1262-1267
Author(s):  
Haojun Yang ◽  
Hanyang Liu ◽  
YuWen Jiao ◽  
Jun Qian
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Metabolic Diseases ◽  
Peptide Yy ◽  
The Body ◽  
Wild Type ◽  
L Cells ◽  
Body Weights ◽  
Gastrointestinal Bypass ◽  
G Protein Coupled

Background: G protein-coupled bile acid receptor (TGR5) is involved in a number of metabolic diseases. The aim of this study was to identify the role of TGR5 after Roux-en-Y gastric bypass (GBP). Methods: Wild type and TGR5 knockout mice (tgr5-/-) were fed a high-fat diet (HFD) to establish the obesity model. GBP was performed. The changes in body weight and food intake were measured. The levels of TGR5 and peptide YY (PYY) were evaluated by RT-PCR, Western blot, and ELISA. Moreover, the L-cells were separated from wild type and tgr5-/- mice. The levels of PYY in L-cells were evaluated by ELISA. Results: The body weights were significantly decreased after GBP in wild type mice (p<0.05), but not tgr5-/- mice (p>0.05). Food intake was reduced after GBP in wild type mice, but also not significantly affected in tgr5-/- mice (p>0.05). The levels of PYY were significantly increased after GBP compared with the sham group (p<0.05); however, in tgr5-/- mice the expression of PYY was not significantly affected (p>0.05). After INT-777 stimulation in L-cells obtained from murine intestines, the levels of PYY were significantly increased in L-cells tgr5+/+ (p<0.05). Conclusion: Our study suggests that GBP up-regulated the expression of TGR5 in murine intestines, and increased the levels of PYY, which further reduced food intake and decreased the body weight.

The metabolic regulation of fenofibrate is dependent on dietary protein content in male juveniles of Nile tilapia (Oreochromis niloticus)

2019 ◽  
Vol 122 (6) ◽  
pp. 648-656 ◽  
Author(s):  
L. Ning ◽  
Y. Liu ◽  
W. Wang ◽  
Y. Li ◽  
L. Chen ◽  
...  
Keyword(s):  
Dietary Protein ◽  
Nile Tilapia ◽  
Metabolic Regulation ◽  
Energy Content ◽  
High Energy ◽  
The Body ◽  
Lipid Lowering ◽  
Hepatosomatic Index ◽  
Physiological Status ◽  
Dietary Nutrient

AbstractThe fenofibrate functions in mammals could be affected by many factors such as dietary nutrient levels and physiological status. However, this phenomenon has not been well studied in fish. The goal of our study was to investigate the effect of dietary protein contents on metabolic regulation of fenofibrate in Nile tilapia. An 8-week experiment was conducted to feed fish with four diets at two protein levels (28 and 38 %) with or without the supplementation of fenofibrate (200 mg/kg body weight per d). After the trial, the body morphometric parameters, plasma biochemical parameters and quantitative PCR data were examined. These results showed that fenofibrate significantly reduced the feeding intake and weight gain rate, increased the oxidative stress (increased plasma methane dicarboxylic aldehyde) and liver : body ratio (increased hepatosomatic index) in the low protein (LP)-fed fish. In contrast, fenofibrate exhibited a lipid-lowering (reduced hepatic lipid) effect and up-regulated the expressions of the genes related to lipid catabolism, transport and anabolic metabolism in the high protein (HP)-fed fish. The present study suggested that lipid-lowering effect of fenofibrate would be strengthened in the fish fed with the HP diet containing high energy, but in the fish fed with the LP diet containing low energy, the fenofibrate treatment would cause adverse effects for metabolism. Taking together, our study showed that the metabolic regulation of fenofibrate in Nile tilapia was dependent not only on feed energy content but also on dietary nutrient composition, such as dietary protein and/or lipid levels.

scholarly journals Mediators of Host–Microbe Circadian Rhythms in Immunity and Metabolism

Biology ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 417
Author(s):  
Katya Frazier ◽  
Mary Frith ◽  
Dylan Harris ◽  
Vanessa A. Leone
Keyword(s):  
Immune System ◽  
Circadian Rhythms ◽  
Metabolic Regulation ◽  
Metabolic Networks ◽  
Metabolic Diseases ◽  
Biological Rhythms ◽  
Metabolic Health ◽  
Host Immune System ◽  
Gut Microbes ◽  
Communication Modalities

Circadian rhythms are essential for nearly all life forms, mediated by a core molecular gene network that drives downstream molecular processes involved in immune function and metabolic regulation. These biological rhythms serve as the body’s metronome in response to the 24-h light:dark cycle and other timed stimuli. Disrupted circadian rhythms due to drastic lifestyle and environmental shifts appear to contribute to the pathogenesis of metabolic diseases, although the mechanisms remain elusive. Gut microbiota membership and function are also key mediators of metabolism and are highly sensitive to environmental perturbations. Recent evidence suggests rhythmicity of gut microbes is essential for host metabolic health. The key molecular mediators that transmit rhythmic signals between microbes and host metabolic networks remain unclear, but studies suggest the host immune system may serve as a conduit between these two systems, providing homeostatic signals to maintain overall metabolic health. Despite this knowledge, the precise mechanism and communication modalities that drive these rhythms remain unclear, especially in humans. Here, we review the current literature examining circadian dynamics of gut microbes, the immune system, and metabolism in the context of metabolic dysregulation and provide insights into gaps and challenges that remain.

scholarly journals Amino Acid Sensing in Metabolic Homeostasis and Health

2020 ◽  
Author(s):  
Xiaoming Hu ◽  
Feifan Guo
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Metabolic Regulation ◽  
Metabolic Diseases ◽  
Nutrient Sensing ◽  
The Body ◽  
Bioactive Molecules ◽  
Metabolic Homeostasis ◽  
Amino Acid Availability ◽  
Amino Acid Sensing

Abstract Sensing and responding to changes in nutrient levels, including those of glucose, lipids, and amino acids, by the body is necessary for survival. Accordingly, perturbations in nutrient sensing are tightly linked with human pathologies, particularly metabolic diseases such as obesity, type 2 diabetes mellitus, and other complications of metabolic syndromes. The conventional view is that amino acids are fundamental elements for protein and peptide synthesis, while recent studies have revealed that amino acids are also important bioactive molecules that play key roles in signaling pathways and metabolic regulation. Different pathways that sense intracellular and extracellular levels of amino acids are integrated and coordinated at the organismal level, and, together, these pathways maintain whole metabolic homeostasis. In this review, we discuss the studies describing how important sensing signals respond to amino acid availability and how these sensing mechanisms modulate metabolic processes, including energy, glucose, and lipid metabolism. We further discuss whether dysregulation of amino acid sensing signals can be targeted to promote metabolic disorders, and discuss how to translate these mechanisms to treat human diseases. This review will help to enhance our overall understanding of the correlation between amino acid sensing and metabolic homeostasis, which have important implications for human health.

Melatonin and Oxidative Stress in the Diabetic State: Clinical Implications and Potential Therapeutic Applications

2019 ◽  
Vol 26 (22) ◽  
pp. 4178-4190 ◽  
Author(s):  
Javier Espino ◽  
Ana B. Rodríguez ◽  
José A. Pariente
Keyword(s):  
Oxidative Stress ◽  
Circadian Rhythms ◽  
Antioxidant Capacity ◽  
Metabolic Diseases ◽  
Association Studies ◽  
Genetic Association Studies ◽  
Metabolic Disturbances ◽  
Increased Risk ◽  
Living Organisms

All living organisms exhibit circadian rhythms, which govern the majority of biological functions, including metabolic processes. Misalignment of these circadian rhythms increases the risk of developing metabolic diseases. Thus, disruption of the circadian system has been proven to affect the onset of type 2 diabetes mellitus (T2DM). In this context, the pineal indoleamine melatonin is a signaling molecule able to entrain circadian rhythms. There is mounting evidence that suggests a link between disturbances in melatonin production and impaired insulin, glucose, lipid metabolism, and antioxidant capacity. Besides, several genetic association studies have causally associated various single nucleotide polymorphysms (SNPs) of the human MT2 receptor with increased risk of developing T2DM. Taken together, these data suggest that endogenous as well as exogenous melatonin may influence diabetes and associated metabolic disturbances not only by regulating insulin secretion but also by providing protection against reactive oxygen species (ROS) since pancreatic &#946;-cells are very susceptible to oxidative stress due to their low antioxidant capacity.

scholarly journals Suprachiasmatic vasopressin to paraventricular oxytocin neurocircuit in the hypothalamus relays light reception to inhibit feeding behavior

2018 ◽  
Vol 315 (4) ◽  
pp. E478-E488 ◽  
Author(s):  
Putra Santoso ◽  
Masanori Nakata ◽  
Yoichi Ueta ◽  
Toshihiko Yada
Keyword(s):  
Food Intake ◽  
Circadian Rhythms ◽  
Feeding Behavior ◽  
Metabolic Diseases ◽  
Light Exposure ◽  
Firing Frequency ◽  
Dark Phase ◽  
The Novel ◽  
Intracellular Ca ◽  
Anorexigenic Effect

Light synchronizes the body’s circadian rhythms by modulating the master clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus. In modern lifestyles that run counter to normal circadian rhythms, the extended and/or irregular light exposure impairs circadian rhythms and, consequently, promotes feeding and metabolic disorders. However, the neuronal pathway through which light is coupled to feeding behavior is less elucidated. The present study employed the light exposure during the dark phase of the day in rats and observed its effect on neuronal activity and feeding behavior. Light exposure acutely suppressed food intake and elevated c-Fos expression in the AVP neurons of SCN and the oxytocin (Oxt) neurons of paraventricular nucleus (PVN) in the hypothalamus. The light-induced suppression of food intake was abolished by blockade of the Oxt receptor in the brain. Retrograde tracer analysis demonstrated the projection of SCN AVP neurons to the PVN. Furthermore, intracerebroventricular injection of AVP suppressed food intake and increased c-Fos in PVN Oxt neurons. Intra-PVN injection of AVP exerted a stronger anorexigenic effect than intracerebroventriclar injection. AVP also induced intracellular Ca2+ signaling and increased firing frequency in Oxt neurons in PVN slices. These results reveal the novel neurocircuit from SCN AVP to PVN Oxt that relays light reception to inhibition of feeding behavior. This light-induced neurocircuit may serve as a pathway for forming the circadian feeding rhythm and linking irregular light exposure to arrhythmic feeding and, consequently, obesity and metabolic diseases.

scholarly journals Dancing to circadian rhythms: microbes and metabolism

2017 ◽  
Vol 39 (2) ◽  
pp. 30-33
Author(s):  
Mrinalini C. Rao ◽  
Eugene B. Chang
Keyword(s):  
Circadian Rhythms ◽  
Gut Microbiome ◽  
Metabolic Health ◽  
The Body ◽  
Bioactive Molecules ◽  
Negative Consequences ◽  
Metabolic Disturbances ◽  
Metabolic Functions ◽  
Distant Organ ◽  
Host Metabolism

Since the turn of the 21st century, two advances in biology have revolutionized our thinking of human metabolism. First, is the in-depth characterization of a previously recognized, but hitherto poorly defined organ system, the gut microbiome. This microbial organ exquisitely interacts with the diet which greatly influences its metabolic functions to impact host metabolism through the production of small bioactive molecules that continuously enter the bloodstream to act at local and distant organ tissues. Equally important, the host metabolism can also modulate the gut microbiome setting up the two as intricate and well-suited partners. Second, is the recognition that most of the cells and organs of the body are dependent on circadian rhythms, systemic timekeepers that play a major role in regulating behavioural and physiological functions to manage energy balance. In conditions of metabolic health, circadian rhythms are the beat to which the two well-matched partners, microbes and metabolism, dance. When these partners are out of step or mismatched, negative consequences may develop that promote metabolic disturbances and disease. Thus, unravelling this complex choreography becomes key to understanding how to maintain metabolic health and to correct missteps that may lead to the development of conditions like diet-induced obesity.

scholarly journals Distribution and function of glucagon-like peptide 1 (GLP-1) in the digestive tract of mammals and the clinical use of its analogues

2023 ◽  
Vol 76 (07) ◽  
pp. 6374-2023 ◽  
Author(s):  
ALEKSANDRA GÓRSKA ◽  
MARCIN B. ARCISZEWSKI
Keyword(s):  
Type 2 Diabetes ◽  
Food Intake ◽  
Metabolic Diseases ◽  
Biological Effects ◽  
Glucagon Secretion ◽  
The Body ◽  
Reactive Hypoglycemia ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Recently, interest in glucagon-like peptide-1 (GLP-1) and other peptides derived from preproglucagon has increased significantly. GLP-1 is a 30-amino acid peptide hormone produced in L-type enteroendocrine cells as a response to food intake. GLP-1 is rapidly metabolized and inactivated by the dipeptidyl peptidase IV enzyme before the hormone leaves the intestine, which increases the likelihood that GLP-1 action is transmitted through sensory neurons in the intestine and liver through the GLP-1 receptor. The main actions of GLP-1 are to stimulate insulin secretion (i.e. act as incretin hormone) and inhibit glucagon secretion, thus contributing to the reduction of postprandial glucose spikes. GLP-1 also inhibits motility and gastrointestinal secretion, and therefore acts as part of the „small bowel brake” mechanism. GLP-1 also appears to be a physiological regulator of appetite and food intake. Because of these effects, GLP-1 or GLP-1 receptor agonists are now increasingly used to treat type 2 diabetes. Reduced GLP-1 secretion may contribute to the development of obesity, and excessive secretion may be responsible for postprandial reactive hypoglycemia. The use of GLP-1 agonists opens up new possibilities for the treatment of type 2 diabetes and other metabolic diseases. In the last two decades, many interesting studies covering both the physiological and pathophysiological role of GLP-1 have been published, and our understanding of GLP-1 has broadened significantly. In this review article, we have tried to describe our current understanding of how GLP-1 works as both a peripheral hormone and as a central neurotransmitter in health and disease. We focused on its biological effects on the body and the potential clinical application in relation to current research.

scholarly journals Uroguanylin Improves Leptin Responsiveness in Diet-Induced Obese Mice

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 752 ◽  
Author(s):  
Cintia Folgueira ◽  
Daniel Beiroa ◽  
María González-Rellán ◽  
Begoña Porteiro ◽  
Edward Milbank ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Metabolic Regulation ◽  
Energy Homeostasis ◽  
Molecular Mechanisms ◽  
The Body ◽  
Leptin Sensitivity ◽  
Homeostasis Regulation ◽  
Transcription 3 ◽  
Hypothalamic Level

The gastrointestinal-brain axis is a key mediator of the body weight and energy homeostasis regulation. Uroguanylin (UGN) has been recently proposed to be a part of this gut-brain axis regulating food intake, body weight and energy expenditure. Expression of UGN is regulated by the nutritional status and dependent on leptin levels. However, the exact molecular mechanisms underlying this UGN-leptin metabolic regulation at a hypothalamic level still remains unclear. Using leptin resistant diet-induced obese (DIO) mice, we aimed to determine whether UGN could improve hypothalamic leptin sensitivity. The present work demonstrates that the central co-administration of UGN and leptin potentiates leptin’s ability to decrease the food intake and body weight in DIO mice, and that UGN activates the hypothalamic signal transducer and activator of transcription 3 (STAT3) and phosphatidylinositide 3-kinases (PI3K) pathways. At a functional level, the blockade of PI3K, but not STAT3, blunted UGN-mediated leptin responsiveness in DIO mice. Overall, these findings indicate that UGN improves leptin sensitivity in DIO mice.

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