OBJECTIVE: Here, we present a systematic review that compiles in vivo experimental data regarding the effect of the WD on the gut microbiota and its impact on the circadian rhythm. Additionally, we reviewed studies evaluating the combined effects of WD and circadian cycle disruption on gut microbiota and circadian cycle markers.
METHODS: The original studies indexed in PubMed/Medline, Scopus, and Web of Science databases were screened according to the PRISMA strategy.
RESULTS: Preclinical studies revealed that WD triggers circadian rhythmicity disruption, reduces the alpha-diversity of the microbiota and favors the growth of bacterial groups that are detrimental to intestinal homeostasis, such as Clostridaceae, Enterococcus, Parasutterella and Proteobacteria. When the WD is combined with circadian clock disruption, gut dysbiosis become more pronounced. Reduced cycling of Per3, Rev-erb and CLOCK in the intestine, which are related to dysregulation of lipid metabolism and potential metabolic disease, was observed.
CONCLUSIONS: In conclusion, current evidence supports the potential of WD to trigger microbiota dysregulation, disrupt the biological clock, and increase susceptibility to metabolic disorders and potentially chronic diseases.

Plant-rich diets (PRDs), also referred to as plant based diets, have been shown to have beneficial effects on various chronic diseases and all-cause mortality. However, limited data are available on the effect of such diets on sleep and sleep disorders. In this review article, we explore existing evidence and potential mechanisms by which PRDs may impact sleep and sleepiness. High-fat diets are associated with drowsiness, while fiber-rich diets improve sleep quality. Anti-inflammatory diets may benefit patients with sleep disturbances, and diets rich in tryptophan and serotonin precursors may improve sleep quality. Isoflavones and polyphenols present in PRDs may also have a positive impact on sleep. Furthermore, diets rich in plants may reduce the risk of obstructive sleep apnea and associated daytime sleepiness. Overall, the current knowledge about PRDs in sleep and sleep disorders is limited, and further research is needed to explore the potential advantages of this dietary approach in sleep disorders.

Oxidative stress is a major cellular event that occurs in the placenta, fulfilling critical physiological roles in non-pathological pregnancies. However, exacerbated oxidative stress is a pivotal feature of different obstetric complications, like pre-eclampsia, fetal growth restriction, and other diseases. Compelling evidence supports the relevant role of diet during pregnancy, with pleiotropic consequences for maternal well-being. The present review aims to examine the complex background between oxidative stress and placental development and function in physiological conditions, also intending to understand the relationship between different dietary patterns and the human placenta, particularly how this could influence oxidative stress processes. The effects of Westernized diets (WDs) and high-fat diets (HFDs) rich in ultra-processed foods and different additives are compared with healthy patterns such as a Mediterranean diet (MedDiet) abundant in omega 3 polyunsaturated fatty acids, monounsaturated fatty acids, polyphenols, dietary fiber, and vitamins. Although multiple studies have focused on the role of specific nutrients, mostly in animal models and in vitro, further observational and intervention studies focusing on the placental structure and function in women with different dietary patterns should be conducted to understand the precise influence of diet on this organ.

Cardiovascular diseases (CVD) are the leading cause of death globally, estimated at 17.9 million premature deaths. Several risk factors contribute to the development of CVD, including unhealthy diet rich in saturated fat. Quercetin (Q) is a important natural flavonoid with cardioprotective effect. However, it is crucial to understand and clarify which dosages and intervention times quercetin promotes better cardioprotective effects when exposed to a High-Fat Diet (HFD). We aim was to carry out a review to identify and compare experimental studies that investigated the quercetin effect on cardiac parameters in rodents fed a HFD. This literature search was performed through the specialized databases PubMed, Embase, Web of Science and Lilacs in May 2022. The following information was collected and assessed: Species of animals, dietary fat content, intervention protocol (quercetin), and main results of alterations associated with cardiac change. A total of 116 articles were selected from the database and 30 articles were included in this study. The administration form of quercetin was used in the diet supplemented in 73.4% (n = 22) of the studies. The dosage ranged between 10 and 100 mg/kg, 0.01%-0.36%, and 4-8 g/kg diet. The treatment time ranged between 14 and 63 days in 48.4% studies and most of the selected studies observed changes in the: Serum concentrations of lipids (60%, n = 18) mainly decrease in TC and TG, left ventricle (LV) (16.13%, n = 5) includes attenuation of the cardiac hypertrophy; inhibition of atherosclerotic progression (32%, n = 10) with decrease in lesions and plaque formation; improvement in the expression of gene and protein associated with cardiac functionality and oxidative stress (51.6%; n = 16). Quercetin supplementation at different concentrations/doses promotes important cardioprotective effects in experimental models exposed to a HFD. The supplemented diet was shown to be the better administration option. The methodological variation presented in the articles selected in this review proves that the most appropriate intervention protocol, as well as the most effective route of administration, promotes these effects.

Saturated fats found in diets known as high-fat, cafeteria, or Western diets appear to have a negative effect on bone structure; however, few studies have focused on investigating this association, and the data available in the literature remain controversial.
The aim of the current review was to investigate the effects of a high-fat dietary intake on the bone structure of Wistar rats.
A search for articles was carried out in the Pubmed/MEDLINE, Web of Science, Embase, and Scopus databases.
In total, 447 articles were found in the initial search; 5 articles were included in the systematic review, after application of the exclusion criteria.
The review was guided by the PICOS strategy and based on the PRISMA protocol for animal reviews.
High-fat diets appear to affect bone structure of Wistar rats. Diet composition and exposure time are the factors determining the strength of the effect.

Emerging studies in the literature describe an association between high-fat, low-carbohydrate diets and severe hypercholesterolemia consistent with the levels observed in patients with (homozygous) familial hypercholesterolemia (FH). High levels of low-density lipoprotein cholesterol (LDL-C) may result from the reduced clearance of LDL particles from the circulation, the increased production of their precursor, or a combination of both. The increased intake of (saturated) fat and cholesterol, combined with limited to no intake of carbohydrates and fiber, are the main features of diets linked to hypercholesterolemia. However, several observations in previous studies, together with our observations from our lipid clinic, do not provide a definitive pathophysiological explanation for severe hypercholesterolemia. Therefore, we review these findings and possible pathophysiological explanations as well as opportunities for future research. Altogether, clinicians should rule out high-fat, low-carbohydrate diets as a possible cause for hypercholesterolemia in patients presenting with clinical FH in whom no mutation is found and discuss dietary modifications to durably reduce LDL-C levels and cardiovascular disease risk.

Chronic inflammation refers to long-lasting inflammation that occurs over a period of several months to years, and it is associated with the progression of other chronic diseases. It may be induced by alcohol consumption and a high-fat diet. Soybean bioactive compounds prevent chronic inflammation by primarily targeting the nuclear factor kappa B (NF-κB) pathway, which inhibits the phosphorylation of IkappaB kinase complex (IκB) and reduces inflammatory marker levels. We performed a systematic review of studies published between 2012 and 2022 on the impact of soybeans on diet-induced chronic inflammation. Soy bioactive compounds may mitigate chronic inflammation. However, more human intervention studies are needed to assess their efficacy as potential modulating agents for inflammation and inflammation-related diseases. The objective was to review the impact of soy-derived bioactive compounds on high-fat diet-induced and alcohol-induced inflammation. To our knowledge, it is the first review to look specifically at high-fat diet-induced and alcohol-induced inflammation and how it is modulated by specific bioactive compounds in soybean.

OBJECTIVE: We conducted a meta-analysis to investigate whether diabetes induced by a high-fat diet (HFD) has the potential to alter the process of autophagy in the murine liver.
METHODS: A systematic literature search was performed with electronic databases (PubMed, EMBASE, Web of Science). Study design, population, intervention, outcome, and risk of bias were analyzed. Given the availability of studies, a quantitative meta-analysis including 23 studies was performed.
RESULTS: The search found 5754 articles, with 48 matching the eligibility criteria, comprising of 1033 animals. The meta-analysis showed that diabetic murines fed with HFD presented an absence of p62 degradation (SMD 4.63, 95 % CI 2.02 to 7.24, p = 0.0005; I2 = 77 %), higher expression of p-mTOR/mTOR (SMD 5.20, 95 % CI 1.00 to 9.39, p = 0.01; I2 = 78 %), and a decreased p-AMPK/AMPK ratio (SMD -2.02, 95 % CI -3.96 to -0.09, p = 0.04; I2 = 85 %) when compared to nondiabetic murines. When associated with streptozotocin, the animals presented decreased ATG-7 and LC3-II. The meta-regression results showed a decrease in autophagy responses due to increased glycemic levels, fat content, and long-term exposure to HFD, and advanced animal age. The common and species-specific protein responses were also consistent with the inhibition of autophagy.
CONCLUSIONS: The normal process of autophagy mechanisms in the liver is less competent after HFD consumption. The destabilization of (auto)phagolysosomes contributes to the perpetuation of diabetes, metabolic dysfunction-associated fatty liver disease, and cell death.

Worldwide, infertility affects between 10 and 15% of reproductive-aged couples. Female infertility represents an increasing health issue, principally in developing countries, as the current inclinations of delaying pregnancy beyond 35 years of age significantly decrease fertility rates. Female infertility, commonly imputable to ovulation disorders, can be influenced by several factors, including congenital malformations, hormonal dysfunction, and individual lifestyle choices, such as smoking cigarettes, stress, drug use and physical activity. Moreover, diet-related elements play an important role in the regulation of ovulation. Modern types of diet that encourage a high fat intake exert a particularly negative effect on ovulation, affecting the safety of gametes and the implantation of a healthy embryo. Identifying and understanding the cellular and molecular mechanisms responsible for diet-associated infertility might help clarify the confounding multifaceted elements of infertility and uncover novel, potentially curative treatments. In this view, this systematic revision of literature will summarize the current body of knowledge of the potential effect of high-fat diet (HFD) exposure on oocyte and follicular quality and consequent female reproductive function, with particular reference to molecular mechanisms and pathways. Inflammation, oxidative stress, gene expression and epigenetics represent the main mechanisms associated with mammal folliculogenesis and oogenesis.

Obesity poses deleterious consequences on every organ system, especially the lymphatic network. However, the underlying cellular mechanisms through which obesity causes lymphatic dysfunction remains unclear. We aimed to summarize experimental studies that evaluated the effect of obesity on the lymphatic system on animal models.
We used the following terms to search the Ovid EMBASE, Ovid MEDLINE(R), Cochrane, and Scopus databases: \"lymphedema\", \"lymphatic diseases\", \"lymphatic system/complications* \", \"lymphatic system/injuries* \", \"lymphatic system/abnormalities* \", AND \"obesity/complications* \", \"diet/high-fat\", \"adipogenesis\" and \"lipid metabolism disorder\". From a total of 166 articles identified in the initial search, 13 met our eligibility criteria.
Long-term exposure to high-fat diet in mice demonstrated significant amount of adipose tissue deposition which sets off an inflammatory cascade resulting in disruption of the chemokine gradient, inhibition of lymphangiogenesis, and changes in gene expression of lymphatic endothelial cells, that alter vessel permeability and induce cell death. Reduced contractile properties of lymphatic collectors, dilated capillaries, increased tissue pressure, and reduced hydraulic conductivity collectively contribute to reduced impaired lymphatic drainage. Aerobic exercise has shown reversal of lymphatic dysfunction in the obese and pharmacological interventions targeting T-cells, iNOS and VEGFR-3 signaling have the potential to combat acquired lymphedema.
Scientists should focus their future experiments on developing therapies that regulate expression of T-cell derived cytokines and VEGFR-3 expression whereas clinicians are urged to counsel their patients to reduce weight through aerobic exercise.