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Background Time-restricted feeding is an emerging dietary intervention that is becoming increasingly popular. There are, however, no randomised clinical trials of time-restricted feeding in overweight patients with type 2 diabetes. Here, we explored the effects of time-restricted feeding on glycaemic regulation and weight changes in overweight patients with type 2 diabetes over 12 weeks. Methods Overweight adults with type 2 diabetes (n = 120) were randomised 1:1 to two diet groups: time-restricted feeding (n = 60) or control (n = 60). Sixty patients participated in a 10-h restricted feeding treatment program (ad libitum feeding from 8:00 to 18:00 h; fasting between 18:00 and 8:00 h) for 12 weeks. Results Haemoglobin A1c and body weight decreased in the time-restricted feeding group (− 1.54% ± 0.19 and − 2.98 ± 0.43 kg, respectively) relative to the control group over 12 weeks ( p  < 0.001). Homeostatic model assessment of β-cell function and insulin resistance changed in the time-restricted feeding group (0.73 ± 0.21, p  = 0.005; − 0.51 ± 0.08, p  = 0.02, respectively) compared with the control group. The medication effect score, SF-12 score, and the levels of triglycerides, total cholesterol and low-density lipoprotein cholesterol were improved in the time-restricted feeding group (− 0.66 ± 0.17, p  = 0.006; 5.92 ± 1.38, p  < 0.001; − 0.23 ± 0.08 mmol/L, p  = 0.03; − 0.32 ± 0.07 mmol/L, p  = 0.01; − 0.42 ± 0.13 mmol/L, p  = 0.02, respectively) relative to the control group. High-density lipoprotein cholesterol was not significantly different between the two groups. Conclusion These results suggest that 10-h restricted feeding improves blood glucose and insulin sensitivity, results in weight loss, reduces the necessary dosage of hypoglycaemic drugs and enhances quality of life. It can also offer cardiovascular benefits by reducing atherosclerotic lipid levels. Trial registration : This study was registered with the Chinese Clinical Trial Registry (ChiCTR-IPR-15006371).

Time‐restricted feeding (TRF) holds promise for alleviating cognitive decline in aging, albeit the precise mechanism via the gut‐brain axis remains elusive. In a clinical trial, we observed, for the first time, that a 4‐month TRF ameliorated cognitive impairments among Alzheimer's disease (AD) patients. Experiments in 5xFAD mice corroborated the gut microbiota‐dependent effect of TRF on mitigating cognitive dysfunction, amyloid‐beta deposition, and neuroinflammation. Multi‐omics integration linked Bifidobacterium pseudolongum (B. pseudolongum) and propionic acid (PA) with key genes in AD pathogenesis. Oral supplementation of B. pseudolongum or PA mimicked TRF's protective effects. Positron emission tomography imaging confirmed PA's blood‐brain barrier penetration, while knockdown of the free fatty acid receptor 3 (FFAR3) diminished TRF's cognitive benefits. Notably, we observed a positive correlation between fecal PA and improved cognitive function in an AD cohort, further indicating that TRF enhanced PA production. These findings highlight the microbiota‐metabolites‐brain axis as pivotal in TRF's cognitive benefits, proposing B. pseudolongum or PA as potential AD therapies. A 4‐month of time‐restricted feeding (TRF) intervention alleviated cognitive impairments in Alzheimer's disease (AD) patients, while a 3‐month TRF regimen improved spatial memory, reduced amyloid‐beta accumulation, and promoted microglial aggregation around plaques in AD mice. Antibiotic‐induced gut microbiota depletion partly abolished TRF's benefits. Through creatively integrating gut microbiota, metabolites, and hippocampal genes, Bifidobacterium pseudolongum (B. pseudolongum) and propionic acid (PA) were identified as key contributors to TRF's cognitive effects, with supplementation of either mimicking TRF's protective benefits. Positron emission tomography imaging revealed that PA directly crossed the blood‐brain barrier, and PA supplementation restored disrupted metabolism in AD mice. Knockdown of its receptor free fatty acid receptor 3 (FFAR3) diminished TRF's protective effects. A case‐control study showed a negative association between PA and cognitive status, while the TRF clinical intervention linked fecal PA to cognitive status. These findings suggest PA as a potential biomarker and underscore precise TRF‐based nutritional interventions as a promising strategy for managing neurodegenerative diseases. Highlights Time‐restricted feeding (TRF) improved cognitive function in Alzheimer's disease (AD) patients, with notable enhancement in executive function. Multi‐omics integrated analysis in AD mice identified Bifidobacterium pseudolongum (B. pseudolongum) and propionic acid (PA) as key mediators of TRF's cognitive benefits. The potential molecular mechanism by which TRF alleviates cognitive impairment induced by AD involves the B. pseudolongum–PA‐free fatty acid receptor 3 (FFAR3) pathway. Case‐control study and TRF clinical intervention demonstrated PA as a potential biomarker for AD.

•The time-restricted feeding group had a distinct microbial abundance at genus, phylum, and family levels compared with the non–time-restricted feeding group.•There was a significant proportion difference in gut microbiota between the time-restricted feeding group and the non–time-restricted feeding group.•Dietary nutrient intake significantly correlates with microbial richness and abundance. Objectives: Time-restricted feeding (TRF) is a dietary therapeutic remedy for the prevention and treatment of metabolic diseases. Gut microbiota may influence the host metabolism and nutritional status of individuals. Given the significance of TRF and gut microbiota in metabolic diseases, the aim of this study was to explore the association between TRF and gut microbiota in healthy individuals, which is not clearly elucidated. Methods: Thirty healthy men (18–30 y of age) were divided in to two groups (TRF: n = 15 and non-TRF: n = 15). The TRF group was instructed to not consume any food for 16 h/d. Two-day food diary was used for dietary data collection. Stool samples were collected from both groups after 25 d of TRF or non-TRF. Gut microbiota profile was analyzed and quantified by using 16S rRNA gene sequencing. Results: Cluster analysis revealed that Prevotlla_9, Faecalibacterium, and Dialister were the most abundant species in TRF, whereas Prevotell_7, Alloprevotella, and Prevotella_2 were less abundant in the non-TRF group. At the genus level, gut microbiota of the TRF group was significantly changed compared with that of the non-TRF group. Moreover, bar plot analysis revealed that Bacteroidetes was the most abundant phylum in TRF group, followed by Firmicutes. Heat map correlation showed that polyunsaturated fatty acids and vitamin D were positively correlated with Firmicutes, whereas iodine, vitamin E, magnesium, and carbohydrate intake were negative correlated with microbial richness. Conclusion: The present study demonstrated that TRF is associated with microbial composition and relative abundance. TRF intervention might increase microbial abundance, thereby influencing the host metabolism and nutritional status.

Time-restricted feeding (TRF) limits the time and duration of food availability without calorie reduction. Although a high-fat (HF) diet leads to disrupted circadian rhythms, TRF can prevent metabolic diseases, emphasizing the importance of the timing component. However, the question of when to implement the feeding window and its metabolic effect remains unclear, specifically in obese and metabolically impaired animals. Our aim was to study the effect of early vs. late TRF-HF on diet-induced obese mice in an 8:16 light–dark cycle. C57BL male mice were fed ad libitum a high-fat diet for 14 weeks after which they were given the same food during the early (E-TRF-HF) or late (L-TRF-HF) 8 h of the dark phase for 5 weeks. The control groups were fed ad libitum either a high-fat (AL-HF) or a low-fat diet (AL-LF). Respiratory exchange ratio (RER) was highest for the AL-LF group and the lowest for the AL-HF group. E-TRF-HF led to lower body weight and fat depots, lower glucose, C-peptide, insulin, cholesterol, leptin, TNFα, and ALT levels compared with L-TRF-HF- and AL-HF-fed mice. TRF-HF regardless whether it was early or late led to reduced inflammation and fat accumulation compared with AL-HF-fed mice. E-TRF-HF led to advanced liver circadian rhythms with higher amplitudes and daily expression levels of clock proteins. In addition, TRF-HF led to improved metabolic state in muscle and adipose tissue. In summary, E-TRF-HF leads to increased insulin sensitivity and fat oxidation and decreased body weight, fat profile and inflammation contrary to AL-HF-fed, but comparable to AL-LF-fed mice. These results emphasize the importance of timed feeding compared to ad libitum feeding, specifically to the early hours of the activity period.

Overnutrition is a risk factor for various human diseases, including neurodegenerative diseases, metabolic disorders, and cancers. Therefore, targeting overnutrition represents a simple but attractive strategy for the treatment of these increasing public health threats. Fasting as a dietary intervention for combating overnutrition has been extensively studied. Fasting has been practiced for millennia, but only recently have its roles in the molecular clock, gut microbiome, and tissue homeostasis and function emerged. Fasting can slow aging in most species and protect against various human diseases, including neurodegenerative diseases, metabolic disorders, and cancers. These centuried and unfading adventures and explorations suggest that fasting has the potential to delay aging and help prevent and treat diseases while minimizing side effects caused by chronic dietary interventions. In this review, recent animal and human studies concerning the role and underlying mechanism of fasting in physiology and pathology are summarized, the therapeutic potential of fasting is highlighted, and the combination of pharmacological intervention and fasting is discussed as a new treatment regimen for human diseases. Fasting is emerging as a simple but attractive strategy for fighting human diseases, including aging, cancer, neurodegenerative diseases, and metabolic disorders. This review provides an a timely overview of the role and mechanism of fasting in physiology and pathology, highlights the therapeutic potential of fasting, alone and in combination with pharmacological intervention, and discusses the current challenges and prospects.

Recent research has highlighted the essential role of the microbiome in maintaining skeletal muscle physiology. The microbiota influences muscle health by regulating lipid metabolism, protein synthesis, and insulin sensitivity. However, metabolic disturbances such as obesity can lead to dysbiosis, impairing muscle function. Time‐restricted feeding (TRF) has been shown to mitigate obesity‐related muscle dysfunction, but its effects on restoring healthy microbiomes remain poorly understood. This study utilizes 16S microbiome analysis and bacterial supplementation to investigate the bacterial communities influenced by TRF that may benefit skeletal muscle physiology. In wild‐type and obese Drosophila models (axenic models devoid of natural microbial communities), the absence of microbiota influence muscle performance and metabolism differently. Specifically, axenic wild‐type Drosophila exhibited reduced muscle performance, higher glucose levels, insulin resistance, ectopic lipid accumulation, and decreased ATP levels. Interestingly, in obese Drosophila (induced by a high‐fat diet or predisposed obesity mutant Sk2), the absence of microbiota improved muscle performance, lowered glucose levels, reduced insulin resistance, and increased ATP levels. TRF was found to modulate microbiota composition, notably increasing Acetobacter pasteurianus (AP) and decreasing Staphylococcus aureus (SA) in both obesity models. Supplementation with AP improved muscle performance and reduced glucose and insulin resistance, while SA supplementation had the opposite effect. This study provides novel insights into the complex interactions between TRF, microbiota, and skeletal muscle physiology in different Drosophila models. Time‐restricted feeding (TRF) impacts skeletal muscle physiology and metabolism through microbiome modulation. In Drosophila models, TRF altered microbiota composition, increasing beneficial Acetobacter pasteurianus (AP) and reducing harmful Staphylococcus aureus (SA). AP supplementation improved muscle performance and metabolic health, while SA worsened them. This study highlights the complex interactions between TRF, microbiota, and muscle health, offering insights into obesity‐related muscle dysfunction and potential therapeutic strategies.

Aging and obesity increase multimorbidity and disability risk, and determining interventions for reversing healthspan decline is a critical public health priority. Exercise and time‐restricted feeding (TRF) benefit multiple health parameters when initiated in early life, but their efficacy and safety when initiated at older ages are uncertain. Here, we tested the effects of exercise versus TRF in diet‐induced obese, aged mice from 20 to 24 months of age. We characterized healthspan across key domains: body composition, physical, metabolic, and cardiovascular function, activity of daily living (ADL) behavior, and pathology. We demonstrate that both exercise and TRF improved aspects of body composition. Exercise uniquely benefited physical function, and TRF uniquely benefited metabolism, ADL behavior, and circulating indicators of liver pathology. No adverse outcomes were observed in exercised mice, but in contrast, lean mass and cardiovascular maladaptations were observed following TRF. Through a composite index of benefits and risks, we conclude the net healthspan benefits afforded by exercise are more favorable than those of TRF. Extrapolating to obese older adults, exercise is a safe and effective option for healthspan improvement, but additional comprehensive studies are warranted before recommending TRF. Schafer et al. compare the effects of exercise versus time‐restricted feeding (TRF) on body composition, physical, metabolic, and cardiovascular function, activity of daily living behavior, and pathology in aged, obese mice. They demonstrate that both interventions confer net healthspan benefits, but TRF also drives maladaptive outcomes.

Circadian disruption is associated with an increased risk of cardiometabolic disorders and cardiac diseases. Time‐restricted feeding/eating (TRF/TRE), restricting food intake within a consistent window of the day, has shown improvements in heart function from flies and mice to humans. However, whether and how TRF still conveys cardiac benefits in the context of circadian disruption remains unclear. Here, we demonstrate that TRF sustains cardiac performance, myofibrillar organization, and regulates cardiac lipid accumulation in Drosophila when the circadian rhythm is disrupted by constant light. TRF induces oscillations in the expression of genes associated with triglyceride metabolism. In particular, TRF induces diurnal expression of diacylglycerol O‐acyltransferase 2 (Dgat2), peaking during the feeding period. Heart‐specific manipulation of Dgat2 modulates cardiac function and lipid droplet accumulation. Strikingly, heart‐specific overexpression of human Dgat2 at ZT 0–10 significantly improves cardiac performance in flies exposed to constant light. We have demonstrated that TRF effectively attenuates cardiac decline induced by circadian disruption. Moreover, our data suggests that diurnal expression of Dgat2 induced by TRF is beneficial for heart health under circadian disruption. Overall, our findings have underscored the relevance of TRF in preserving heart health under circadian disruptions and provided potential targets, such as Dgat2, and strategies for therapeutic interventions in mitigating cardiac aging, metabolic disorders, and cardiac diseases in humans. TRF mitigates aging and circadian rhythm disruption cardiac dysfunction including maintaining myofibrillar organization and lipid metabolism. TRF induces the expression rhythmicity of genes linked with triglyceride metabolism and induces diurnal expression of Dgat2 with peak expression during the feeding phase under circadian rhythm disruption. Diurnal expression Overexpression of hDgat2 improves cardiac function under circadian disruption.

Emerging evidence suggests that the timing of eating and exercise over the course of the day is paramount to metabolism and physical function. This review highlights seminal studies showing that adipocyte AMPKα2 signaling controls circadian adipose tissue–skeletal muscle communication. Day-restricted feeding has been shown to improve exercise performance via adipocyte-specific activation of AMPKα2, which controls fat–muscle crosstalk in a time-of-day dependent manner. This review also discusses corroborating experimental studies designating mesenchymal stem cells as key cellular mediators, showing that exercise in the afternoon leads to better metabolic effects in humans, and illustrating how incorrect timing of food intake leads to leptin resistance and metabolic dysregulation. Multi-omics strategies have shed light on the molecular mechanisms underlying such effects of time, showing the circadian control of metabolic processes across tissues. These results advance our knowledge of chronometabolism and offer exciting temporal intervention treatments for metabolic diseases, such as time-restricted feeding, timed exercise, and chronopharmacological targeting of AMPK. Fat–muscle crosstalk, physical performance, and metabolic health outcomes can possibly be optimized by synchronizing dietary and exercise timing with endogenous circadian rhythms.

Disruptions to circadian rhythm may be implicated in the pathogenesis of metabolic syndrome (Met‐S). For example, eating during an extended period of the day may negatively impact the circadian rhythms governing metabolic control, contributing, therefore, to Met‐S and associated end‐organ damage. Accordingly, time‐restricted eating (TRE)/feeding (TRF) is gaining popularity as a dietary intervention for the treatment and prevention of Met‐S. To date, no studies have specifically examined the impact of TRE/TRF on the renal consequences of Met‐S. The proposed study seeks to use a model of experimental Met‐S‐associated kidney disease to address this knowledge gap, disambiguating therein the effects of calorie restriction from the timing of food intake. Spontaneously hypertensive rats will consume a high‐fat diet (HFD) for 8 weeks and then be allocated by stratified randomisation according to albuminuria to one of three groups. Rats will have free 24‐h access to HFD (Group A), access to HFD during the scheduled hours of darkness (Group B) or access to HFD provided in the form of two rations, one provided during the light phase and one provided during the dark phase, equivalent overall in quantity to that consumed by rats in Group B (Group C). The primary outcome measure will be a change in albuminuria. Changes in food intake, body weight, blood pressure, glucose tolerance, fasting plasma insulin, urinary excretion of C‐peptide and renal injury biomarkers, liver and kidney histopathology and inflammation, and fibrosis‐related renal gene expression will be assessed as secondary outcomes.