Similar Datasets
Project description:A ketogenic diet prevents metabolic switching durng time restricted feeding
| PRJNA1043176 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-11-24 | GSE182938 | GEO
Project description:While diet-induced obesity has been exclusively attributed to increased caloric intake from fat, animals fed a high-fat diet (HFD) ad libitum (ad lib) eat frequently throughout day and night, disrupting the normal feeding cycle. To test whether obesity and metabolic diseases result from HFD or disruption of metabolic cycles, we subjected mice to either ad lib or time-restricted feeding (tRF) of a HFD for 8 hr per day. Mice under tRF consume equivalent calories from HFD as those with ad lib access yet are protected against obesity, hyperinsulinemia, hepatic steatosis, and inflammation and have improved motor coordination. The tRF regimen improved CREB, mTOR, and AMPK pathway function and oscillations of the circadian clock and their target genes' expression. These changes in catabolic and anabolic pathways altered liver metabolome and improved nutrient utilization and energy expenditure. We demonstrate in mice that tRF regimen is a nonpharmacological strategy against obesity and associated diseases.
| S-EPMC3491655 | biostudies-literature
Project description:Increased susceptibility of circadian clock mutant mice to metabolic diseases has led to the idea that a molecular clock is necessary for metabolic homeostasis. However, these mice often lack a normal feeding-fasting cycle. We tested whether time-restricted feeding (TRF) could prevent obesity and metabolic syndrome in whole-body Cry1;Cry2 and in liver-specific Bmal1 and Rev-erbα/β knockout mice. When provided access to food ad libitum, these mice rapidly gained weight and showed genotype-specific metabolic defects. However, when fed the same diet under TRF (food access restricted to 10 hr during the dark phase) they were protected from excessive weight gain and metabolic diseases. Transcriptome and metabolome analyses showed that TRF reduced the accumulation of hepatic lipids and enhanced cellular defenses against metabolic stress. These results suggest that the circadian clock maintains metabolic homeostasis by sustaining daily rhythms in feeding and fasting and by maintaining balance between nutrient and cellular stress responses.
| S-EPMC7751278 | biostudies-literature
Project description:Huntington's disease (HD) is a progressive, fatal neurodegenerative disorder with limited treatment options. Substantial evidence implicates mitochondria dysfunction in brain and skeletal muscle in the pathogenesis of HD. Metabolic strategies, such as fasting and ketogenic diets, theoretically enhance brain and muscle metabolism and mitochondria function, which may improve the clinical symptoms of HD. We report the case of a 41-year-old man with progressive, deteriorating HD who pursued a time-restricted ketogenic diet (TRKD) for 48 weeks. Improvements were measured in his motor symptoms (52% improvement from baseline), activities of daily living (28% improvement), composite Unified HD Rating Scale (cUHDRS) score (20% improvement), HD-related behavior problems (apathy, disorientation, anger, and irritability improved by 50-100%), and mood-related quality of life (25% improvement). Cognition did not improve. Weight remained stable and there were no significant adverse effects. This case study is unique in that a patient with progressive, deteriorating HD was managed with a TRKD, with subsequent improvements in his motor symptoms, activities of daily living, cUHDRS score, most major HD-related behavior problems, and quality of life. Our patient remains dedicated to his TRKD, which continues to provide benefit for him and his family.
| S-EPMC9372583 | biostudies-literature
Project description:ObjectiveThe early consumption of calorie-rich diet disrupts circadian rhythms and has adverse effects on memory, yet the effects of time-restricted feeding (TRF) and the underlying molecular mechanisms are unknown. Here, we set out to identify the behavioral and molecular circadian rhythms disruptions generated by juvenile obesogenic diet consumption and their restoration by TRF in male mice.MethodsMetabolic rhythms were measured by indirect calorimetry and memory performances by behavioral tasks. Hippocampal translatome (pS6_TRAP), enrichment and co-regulated gene network analyses were conducted to identify the molecular pathways involved in memory impairments and their restoration by TRF. Differential exon usage analyses, mass spectrometry and pharmacological intervention were used to confirm thyroid hormone signaling involvement.ResultsWe show that four weeks of TRF restore the rhythmicity of metabolic parameters and prevents memory impairments in mice fed a high fat-high sucrose (HFS) diet since weaning, independently of body fat levels. Hippocampal translatome and differential exon usage analyses indicate that impaired memory of mice under ad libitum HFS diet is accompanied by reduced thyroid hormone signaling and altered expression of astrocytic genes regulating glutamate neurotransmission. TRF restored the diurnal expression variation of part of these genes and intra-hippocampal infusion of T3, the active form of thyroid hormone, rescues memory performances and astrocytic gene expression of ad libitum HFS diet-fed mice.ConclusionsThus, thyroid hormones contribute to the TRF positive effects on both metabolism and memory in mice fed an obesogenic diet, highlighting this nutritional approach as a powerful tool in addressing obesity brain comorbidities and paving the way for further mechanistic studies on hippocampal thyroid signaling.
| S-EPMC11609524 | biostudies-literature
Project description:Circadian rhythm disruption (CD) is associated with impaired glucose homeostasis and type 2 diabetes mellitus (T2DM). While the link between CD and T2DM remains unclear, there is accumulating evidence that disruption of fasting/feeding cycles mediates metabolic dysfunction. Here, we used an approach encompassing analysis of behavioral, physiological, transcriptomic, and epigenomic effects of CD and consequences of restoring fasting/feeding cycles through time-restricted feeding (tRF) in mice. Results show that CD perturbs glucose homeostasis through disruption of pancreatic β cell function and loss of circadian transcriptional and epigenetic identity. In contrast, restoration of fasting/feeding cycle prevented CD-mediated dysfunction by reestablishing circadian regulation of glucose tolerance, β cell function, transcriptional profile, and reestablishment of proline and acidic amino acid–rich basic leucine zipper (PAR bZIP) transcription factor DBP expression/activity. This study provides mechanistic insights into circadian regulation of β cell function and corresponding beneficial effects of tRF in prevention of T2DM.
| S-EPMC8673777 | biostudies-literature
Project description:Feeding rodents a high-fat diet (HFD) disrupts normal behavioral rhythms, particularly meal timing. Within the brain, mistimed feeding shifts molecular rhythms in the hippocampus and impairs memory. We hypothesize that altered meal timing induced by an HFD leads to cognitive impairment and that restricting HFD access to the "active period" (i.e., night) rescues the normal hippocampal function. In male mice, ad-lib access to an HFD for 20 weeks increased body weight and fat mass, increased daytime meal consumption, reduced hippocampal long-term potentiation (LTP), and eliminated day/night differences in spatial working memory. Importantly, two weeks of time-restricted feeding (TRF) at the end of the chronic HFD protocol rescued spatial working memory and restored LTP magnitude, even though there was no change in body composition and total daily caloric intake. These findings suggest that short-term TRF is an effective mechanism for rescuing HFD-induced impaired cognition and hippocampal function.
| S-EPMC8188491 | biostudies-literature
Project description:Rheumatoid arthritis (RA) affects approximately 1% of the global population. Its hallmark symptoms include severe pain and joint stiffness, which significantly diminish life quality. RA's development is influenced by multiple factors including unhealthy lifestyle habits. Calorie-rich diets, particularly those high in fat and resulting in obesity, are associated with RA and exacerbate its symptoms. Consequently, dietary modifications are recommended as a complementary treatment. However, adherence is often low due to the restrictive changes required in nutrient composition or caloric intake. Our previous findings indicate that time-restricted feeding (TRF) benefits leukocyte rhythm and mitigates autoimmune responses. In this study we explored the impact of TRF on the severity of K/BxN serum-transfer arthritis (STA) in mice subjected to high-fat diet. Three feeding schedules were implemented: a control (Ctrl) with constant access to standard chow, a high-fat diet group (HF) with ad libitum food access, and a high-fat TRF group (HF-TRF) with a 10-hour feeding window during the active phase. After four weeks of conditioning, STA was induced. Although macroscopic markers of inflammation did not differ between the Ctrl and HF groups, histological analysis revealed increased inflammation in HF mice, including expanded edema, pannus formation, bone erosion, elevated synovial neutrophil infiltration and serum leptin levels. Importantly, all these inflammatory markers were significantly reduced in the HF-TRF group, along with synovial IL-1β and monocyte/macrophage counts. Our results indicate that TRF can diminish the impact of a high-fat diet on STA severity, potentially serving as a preventive method and a sustainable therapeutic support for RA management.
| S-EPMC11864949 | biostudies-literature
Project description:Intermittent fasting (IF) is widely recognized for its numerous health benefits, yet its impact on metabolic health across generations remains relatively unexplored. This study investigates the intergenerational effects of parental IF, specifically through 8-hour daily time-restricted feeding, on the metabolic health of offspring. By examining four different combinations of parental mating groups, we demonstrate that parental IF can influence offspring metabolic health in distinct ways. Our results reveal that parental IF conferred significant metabolic advantages compared to ad libitum (AL) feeding. IF parents exhibited lower glucose, HbA1c, cholesterol, and CRP levels, and higher ketone levels compared to AL parents. Offspring of IF-exposed animals displayed sex-specific metabolic benefits when challenged with a high-fat, high-sugar, and high-salt (HFSS) diet. Notably, female offspring from IF parents were protected against HFSS-induced glucose intolerance and exhibited lower plasma glucose levels and higher ketone levels compared to offspring of ad libitum-fed parents. Additionally, female offspring from IF parents on a HFSS diet, along with both female and male offspring on a normal diet, had elevated plasma insulin levels. Furthermore, male offspring from IF parents on a normal diet exhibited a significant reduction in body weight compared to offspring from AL parents. These findings suggest that parental IF can impart enduring metabolic benefits to offspring and may serve as an effective strategy to mitigate the risks of obesity and diabetes in future generations.
| S-EPMC11900813 | biostudies-literature