scholarly journals Time-Restricted Feeding during Puberty Ameliorates Adiposity and Prevents Hepatic Steatosis in a Mouse Model of Childhood Obesity

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3579
Author(s):  
Francesc Ribas-Aulinas ◽  
Marcela Parra-Vargas ◽  
Marta Ramon-Krauel ◽  
Ruben Diaz ◽  
Carles Lerin ◽  
...  
Keyword(s):  
Childhood Obesity ◽  
Mouse Model ◽  
Hepatic Steatosis ◽  
Caloric Intake ◽  
Total Body Weight ◽  
Metabolic Health ◽  
Dark Phase ◽  
Restricted Feeding ◽  
Dietary Interventions ◽  
Nutritional Interventions

Background: Time restricted feeding (TRF) refers to dietary interventions in which food access is limited during a specific timeframe of the day. TRFs have proven useful in improving metabolic health in adult subjects with obesity. Their beneficial effects are mediated, in part, through modulating the circadian rhythm. Nevertheless, the translation of these dietary interventions onto obese/overweight children and adolescents remains uncharacterized. The objective of this study is to explore the feasibility of temporal dietary interventions for improving metabolic health in the context of childhood obesity. Methods: We have previously developed a mouse model of early adiposity (i.e., childhood obesity) through litter size reduction. Mice raised in small litters (SL) became obese as early as by two weeks of age, and as adults, they developed several obesity-related co-morbidities, including insulin resistance, glucose intolerance and hepatic steatosis. Here, we explored whether two independent short-term chrono-nutritional interventions might improve metabolic health in 1-month-old pre-pubertal SL mice. Both TRFs comprised 8 h feeding/14 h fasting. In the first one (TRF1) Control and SL mice had access to the diet for 8 h during the dark phase. In the second intervention (TRF2) food was available during the light:dark transitions. Results: TRF1 did not alter food intake nor ameliorate adiposity in SL-TRF1. In contrast, SL-TRF2 mice showed unintentional reduction of caloric intake, which was accompanied by reduced total body weight and adiposity. Strikingly, hepatic triglyceride content was completely normalized in SL-TRF1 and SL-TRF2 mice, when compared to the ad lib-fed SL mice. These effects were partially mediated by (i) clock-dependent signals, which might modulate the expression of Pparg or Cpt1a, and (ii) clock-independent signals, such as fasting itself, which could influence Fasn expression. Conclusions: Time-restricted feeding is an effective and feasible nutritional intervention to improve metabolic health, namely hepatic steatosis, in a model of childhood obesity. These data open new avenues for future safe and efficient chrono-nutritional interventions aimed to improve metabolic health in children with overweight/obesity.

scholarly journals Time-restricted feeding improves insulin resistance and hepatic steatosis in a mouse model of postmenopausal obesity

Metabolism ◽  
2016 ◽  
Vol 65 (12) ◽  
pp. 1743-1754 ◽  
Author(s):  
Heekyung Chung ◽  
Winjet Chou ◽  
Dorothy D. Sears ◽  
Ruth E. Patterson ◽  
Nicholas J.G. Webster ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mouse Model ◽  
Hepatic Steatosis ◽  
Restricted Feeding ◽  
Postmenopausal Obesity

scholarly journals 0426 Time Restricted Feeding Consolidates Sleep in the BACHD Mouse Model of Huntington’s Disease

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A163-A163
Author(s):  
I S Nichols ◽  
E Chiem ◽  
Y Tahara ◽  
S Anderson ◽  
D Trotter ◽  
...  
Keyword(s):  
Circadian Rhythms ◽  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Neurodegenerative Disorder ◽  
Nrem Sleep ◽  
Genetic Mutation ◽  
Dark Phase ◽  
Restricted Feeding ◽  
Light Phase

Abstract Introduction Disturbances in the daily sleep-wake cycle are common in individuals with neurodegenerative disorders. Huntington’s disease (HD) is a genetic neurodegenerative disorder in which patients exhibit a variety of impairments that include, poor motor function, disrupted circadian rhythms, and sleep abnormalities such as difficulty initiating sleep at bedtime and more frequent nighttime arousals. In the BACHD mouse model time restricted feeding (TRF) has been successful at improving motor functions and circadian rhythms. The BACHD mouse model has a bacterial artificial chromosome that expresses the full-length human mutant huntingtin gene. Methods In order to determine the effects of TRF on sleep-wake architecture, EEG/EMG polysomnographic records were examined in mice between 3-4 months old bearing the BAC knock-in of a human genetic mutation of HD and WT litter mates, first during ad libitum (ad lib) feeding then during an 18 hour fasting protocol. TRF protocol consisted of 6 hours of food access limited between ZT15-ZT21 and 18 hours of fasting. Results A two-way ANOVA revealed that TRF significantly decreased the amount of total sleep (p=0.04) and NREM sleep (p=0.04) in the dark phase in both WT and BACHD mice. TRF did not significantly affect sleep in the light phase, however trends suggest that BACHD mice have more sleep in the light phase under TRF than ad lib. Conclusion This data suggests that TRF improves sleep by consolidating sleep to the light phase and wake to the dark phase. In conclusion, TRF may be a promising tool that can improve the negative effects of neurodegenerative diseases on sleep-wake processes. Support These experiments were supported by R01-NS078410 and UCLA start-up funds.

Diet and Neurocognition in Mood Disorders - An Overview of the Overlooked

2020 ◽  
Vol 26 (20) ◽  
pp. 2353-2362 ◽  
Author(s):  
Vicent Balanzá-Martínez ◽  
Flavio M. Shansis ◽  
Amparo Tatay-Manteiga ◽  
Pilar López-García
Keyword(s):  
Mood Disorders ◽  
Cognitive Outcomes ◽  
Clinical Staging ◽  
Current Evidence ◽  
Dietary Interventions ◽  
Unhealthy Lifestyle ◽  
Neurocognitive Dysfunction ◽  
Nutritional Interventions ◽  
Lifestyle Choices ◽  
Cognitive Benefits

Bipolar disorder and major depression are associated with significant disability, morbidity, and reduced life expectancy. People with mood disorders have shown higher ratios of unhealthy lifestyle choices, including poor diet quality and suboptimal nutrition. Diet and nutrition impact on brain /mental health, but cognitive outcomes have been less researched in psychiatric disorders. Neurocognitive dysfunction is a major driver of social dysfunction and a therapeutic target in mood disorders, although effective cognitive-enhancers are currently lacking. This narrative review aimed to assess the potential cognitive benefits of dietary and nutritional interventions in subjects diagnosed with mood disorders. Eight clinical trials with nutrients were identified, whereas none involved dietary interventions. Efficacy to improve select cognitive deficits has been reported, but results are either preliminary or inconsistent. Methodological recommendations for future cognition trials in the field are advanced. Current evidence and future views are discussed from the perspectives of precision medicine, clinical staging, nutritional psychiatry, and the brain-gut-microbiota axis.

scholarly journals Metabolism and Aging: New Approaches to Nutrition and Diet in Aging

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 736-737
Author(s):  
Blanka Rogina
Keyword(s):  
Longitudinal Studies ◽  
Calorie Restriction ◽  
Functional Decline ◽  
Metabolic Health ◽  
Tissue Homeostasis ◽  
Nutritional Interventions ◽  
New Approaches ◽  
Nutrition And Diet ◽  
Extended Longevity ◽  
Species Specific

Abstract Aging is associated with a functional decline in metabolic, physiological, proliferative, and tissue homeostasis leading to deterioration at an organismal level and increases risk for disease and death. Genetic, pharmacological and nutritional interventions have been successfully used to preserve metabolic health, which leads to preserved healthspan and extended longevity. This symposium will discuss new approaches to nutrition and diet and mechanisms underlying interventions such as calorie restriction and genetic CR. We will also discuss species-specific metabolic mechanisms based on longitudinal studies in mice, monkeys and humans.

scholarly journals Aberrant Hepatic Expression of PPARγ2 Stimulates Hepatic Lipogenesis in a Mouse Model of Obesity, Insulin Resistance, Dyslipidemia, and Hepatic Steatosis

2006 ◽  
Vol 281 (49) ◽  
pp. 37603-37615 ◽  
Author(s):  
Yuan-Li Zhang ◽  
Antonio Hernandez-Ono ◽  
Patty Siri ◽  
Stuart Weisberg ◽  
Donna Conlon ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mouse Model ◽  
Hepatic Steatosis ◽  
Hepatic Lipogenesis ◽  
Hepatic Expression

Abstract 67: Intervention With Citrus Flavonoids Reverses Existing Metabolic Disorders and Attenuates the Progression of Advanced Atherosclerosis in High Fat--Fed LDLr-/- Mice

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Amy C Burke ◽  
Brian G Sutherland ◽  
Cynthia G Sawyez ◽  
Dawn E Telford ◽  
Joseph Umoh ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Caloric Intake ◽  
Atherosclerotic Lesion ◽  
Lesion Size ◽  
High Fat ◽  
Rapid Weight Gain ◽  
Metabolic Dysregulation ◽  
The Metabolic Syndrome ◽  
Citrus Flavonoids

Previous studies demonstrated that addition of the citrus flavonoids naringenin or nobiletin to a high-fat diet prevented the development of many disorders linked to the metabolic syndrome. In the present study, we assessed the ability of intervention with nobiletin or naringenin to reverse pre-established obesity, insulin resistance, hepatic steatosis, dyslipidemia and attenuate atherogenesis. Ldlr-/- mice were fed chow or a high-fat, cholesterol-containing (HFHC) diet for 12 weeks. For an additional 12 weeks, the HFHC-fed mice: (1) continued on the HFHC diet or were transferred to (2) chow, (3) HFHC + 3% naringenin, or (4) HFHC + 0.3% nobiletin. Following rapid weight gain during HFHC-induction, intervention with naringenin or nobiletin stimulated weight loss, while maintaining caloric intake. Micro-CT imaging revealed flavonoid intervention reversed adipose tissue accumulation by 40-60% in both subcutaneous and visceral depots. At 12 weeks, the HFHC-fed mice were hyperinsulinemic (6-fold), which was accompanied by increased fasting plasma glucose. Intervention with either flavonoid normalized plasma insulin and glucose and corrected impaired insulin and glucose tolerance. The HFHC diet increased cholesterol within VLDL (10-fold) and LDL (6-fold), which was reduced (~50%) by either naringenin or nobiletin intervention. HFHC-induction significantly increased hepatic steatosis. Flavonoid intervention reduced hepatic cholesterol (>50%) and triglyceride (~20%) via increased expression of Pgc1a and Cpt1a and reduced expression of Srebp1c. HFHC-induction increased atherosclerotic lesion area (13-fold), which was increased a further 2.5-fold at 24 weeks. Flavonoid intervention modestly retarded lesion size progression (16-20%). As well, intervention with naringenin or nobiletin slowed the accumulation of aortic cholesterol (~30-45%) and reduced lesional necrotic area (~25%), suggesting improved lesion morphology. These studies demonstrate in mice with pre-existing metabolic dysregulation and atherosclerosis that intervention with naringenin or nobiletin reverses obesity, dyslipidemia, hepatic steatosis and insulin resistance, and modestly attenuates the progression of advanced atherosclerosis.

scholarly journals Time-Restricted Feeding Improves Circadian Dysfunction as well as Motor Symptoms in the Q175 Mouse Model of Huntington’s Disease

eNeuro ◽  
2018 ◽  
Vol 5 (1) ◽  
pp. ENEURO.0431-17.2017 ◽  
Author(s):  
Huei-Bin Wang ◽  
Dawn H. Loh ◽  
Daniel S. Whittaker ◽  
Tamara Cutler ◽  
David Howland ◽  
...  
Keyword(s):  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Motor Symptoms ◽  
Restricted Feeding ◽  
Circadian Dysfunction
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