Could parental high-fat intake program the reproductive health of male offspring? A review.

High-fat diet (HFD) intake can cause overweight and obesity and has become a global public health concern in recent years. Nutritional adversity at vulnerable windows of development can affect developing cells and their functions, including germ cells. Evidence shows that parental HFD intake prior to conception and/or during gestation and lactation could program the reproductive health of male offspring, ultimately resulting in impairment of the first as well as subsequent generations. In male offspring, adipose tissue and hypothalamic-pituitary-gonadal axis imbalance can impair the production of gonadotropins, leading to dysfunction of testosterone production and pubertal onset. The gonads can be directly impaired through oxidative stress, causing poor testosterone production and spermatogenesis; low sperm count, viability, and motility; and abnormal sperm morphology, which results in low sperm quality. Parental HFD intake could also be a risk factor for prostate hyperplasia and cancer in advanced age. It can impact the reproductive pattern of male offspring resulting in impairments in the subsequent generations. The investigation of semen quality must be extended to epidemiological and clinical studies of the male offspring of overweight and/or obese parents in order to improve the quality of human semen. This review addresses the effects of parental HFD intake on the reproductive parameters of male offspring and discusses the possible underlying mechanisms.

IL10/AMPK pathway was associated with the hippocampal anti-inflammatory response to high-sugar and high-fat diet withdrawal.

OBJECTIVE: The present experimental study aimed to evaluate the effect of consuming an obesogenic diet (OD) on serum and hippocampal inflammation and proteins related to energy metabolism, alongside, we evaluated how the same parameters responded to an OD withdrawal. SUBJECTS: Thirty male 60-days-old Wistar rats were used. METHODS: The control group (n = 10) was fed the control diet across the whole experiment. The remaining animals were fed a high-sugar/high-fat (HSHF) diet for 30 days (n = 20) and half of them were placed on the control diet for 48 h (n = 10) afterwards. RESULTS: OD intake decreased hippocampal AMPK phosphorylation, although, it did not increase serum inflammation and only increased hippocampal pNFκBp65 levels without any increase in the cytokines assessed. Moreover, OD withdrawal led to higher inflammatory markers in the serum and hippocampus and higher hippocampal AMPK phosphorylation. The mediation models applied suggested that the effect of OD withdrawal on hippocampal inflammation was driven by serum inflammation, which activated the hippocampal IL10/AMPK anti-inflammatory pathway as a response. CONCLUSION: Our analyses suggest that OD withdrawal increases serum inflammation with hippocampal consequent inflammatory alterations. Despite the general assumption that improving diet improves health, this may not be immediate.

The relationship between serum fatty acids and depressive symptoms in obese adolescents.

Depression and obesity are highly prevalent and are considered inflammatory pathologies; in addition, they are also associated with dietary patterns including types of fatty acids (FA). Changes in the FA composition in the brain are determined by changes in the content and quality of dietary and serum FA. The aim of this study was to verify the relationships between serum-free FA, inflammatory processes and depressive symptoms in obese adolescents. This was a cross-sectional study that analysed a database composed of 138 post-pubertal adolescents. Data regarding the depressive symptoms, body composition, glucose metabolism, lipid profile, FA profile, leptin concentration, as well as adiponectin, IL-A, IL-6, IL-10, TNF-α, C-reactive protein and plasminogen activator inhibitor-1 levels of the subjects were collected. A total of 54·6 % of the adolescents presented with depressive symptoms, and there were positive correlations between depressive symptoms and serum saturated fatty acids (SFA) content, body fat, and inflammatory adipokines, such as leptin, IL-6, and the leptin/adiponectin ratio. Moreover, the content of n-3 polyunsaturated fatty acids (PUFA) was negatively correlated with depressive symptoms, suggesting that eicosatrienoic acid (C20:2n6) and dihomo-γ-linolenic acid (C20:3n-6) are independently associated with depressive symptom scores and can be critical predictors of poor mental health in humans. These results point to the relationship between SFA and depressive symptoms in obese adolescents. However, longitudinal studies are needed to confirm the causality between dietary SFA and depression in obese individuals.

The influence of sex and reproductive cycle on cocaine-induced behavioral and neurobiological alterations: a review.

This systematic review (SR) was aimed at answering two questions: (1) how sex and ovarian hormones alter behavior associated with cocaine use; (2) which possible neurobiological mechanisms explain behavioral differences. Three different researchers conducted a search in PUBMED for all kinds of articles published between the years of 1991 to 2021 on the theme "reproductive cycle and cocaine", "estrous cycle and cocaine", "menstrual cycle and cocaine", "fluctuation of ovarian hormones and cocaine", "estrogen and cocaine" and "progesterone and cocaine". Sixty original studies were identified and subdivided into experimental rodent studies and clinical trials. Experimental studies were characterized by author/year, species/strain, sex/number, age/weight, dose/route/time of administration, hormonal assessment, or administration. Clinical trials were characterized by author/year, sex/number, age, exclusion criterion, dose/route of administration/time of cocaine, and hormonal assessment. Results gathered showed that rodent females develop increased consumption, seeking behavior, craving, relapse, locomotion, increases in stress and anxiety, among other behavioral alterations during peaks of estrogen. These observations are related to the direct effects played by ovarian hormones (in particularly estradiol), in dopamine, but also in serotonin neurons, and in brain regions such as the tegmental area, the nucleus accumbens, the hypothalamus, the amygdala and the prefrontal cortex. Increased sensitization to cocaine presented by high estradiol females was linked to the activation of a CBR1-mediated mechanism and GABA-A-dependent suppression of inhibitory synaptic activity of the prelimbic prefrontal cortex. Estradiol facilitation of cocaine-increased locomotion and self-administration was shown to require the release of glutamate and the activation of metabotropic glutamate receptors subtype 5. Clinical studies also tend to point to a stimulatory effect of estradiol on cocaine sensitization and a neuroprotective effect of progesterone. In conclusion, the results of the present review indicate a need for further preclinical and clinical trials and neurobiological studies to better understand the relationship between sex and ovarian hormones on cocaine sensitization.

Hepatic glycogen participates in the regulation of hypothalamic pAkt/Akt ratio in high-sugar/high-fat diet-induced obesity.

The hypothalamus is a major integrating centre that controls energy homeostasis and plays a major role in hepatic glycogen (HGlyc) turnover. Not only do hypothalamic and hepatic Akt levels influence glucose homeostasis and glycogen synthesis, but exposure to high-sugar/high-fat diets (HSHF) can also lead to hypothalamic inflammation and HGlyc accumulation. HSHF withdrawal overall restores energy and glucose homeostasis, but the actual relationship between hypothalamic inflammation and HGlyc after short-term HSHF withdrawal has not yet been fully elucidated. Here we investigated the short-term effects of HSHF withdrawal preceded by a 30-day HSHF intake on the liver-hypothalamus crosstalk and glucose homeostasis. Sixty-day old male Wistar rats were fed for 30 days a control chow (n = 10) (Ct), or an HSHF diet (n = 20). On the 30th day of dietary intervention, a random HSHF subset (n = 10) had their diets switched to control chow for 48 h (Hw) whilst the remaining HSHF rats remained in the HSHF diet (n = 10) (Hd). All rats were anaesthetized and euthanized at the end of the protocol. We quantified HGlyc, Akt phosphorylation, inflammation and glucose homeostasis biomarkers. We also assessed the effect of propensity to obesity on those biomarkers, as detailed previously. Hd rats showed impaired glucose homeostasis, higher HGlyc and hypothalamic inflammation, and lower pAkt/Akt. Increased HGlyc was significantly associated with HSHF intake on pAkt/Akt lowered levels. We also found that HGlyc breakdown may have prevented a further pAkt/Akt drop after HSHF withdrawal. Propensity to obesity showed no apparent effect on hypothalamic inflammation or glucose homeostasis. Our findings suggest a comprehensive role of HGlyc as a structural and functional modulator of energy metabolism, and such roles may come into play relatively rapidly.

Histopathological and inflammatory response in multiple organs of rats exposed to crack.

The aim of this study was to investigate histopathological and inflammatory response in liver and kidney of rats after crack exposure. For this purpose, a total of 32 male Wistar rats were distributed into four groups: (G1) and (G2): received 18 mg/kg of body weight (b.w) of crack cocaine, but Group G2 remained 72 h without exposure after the experimental period (5 days). Experimental group 3 (G3): received 36 mg/kg of body weight (b.w) of crack cocaine. Control Group (CTRL): received only the vehicle (DMSO) administered by intraperitoneal (i.p) route for 5 days. The results showed that crack cocaine induced histopathological changes in liver and kidney. Immunohistochemistry data revealed that G2 group showed a higher immunoexpression of Ki-67 in hepatic and renal tissues. Regarding inflammation, the results showed that all groups exposed to crack cocaine decreased the expression of TNF-α, IL-6, and IL-10 in liver and kidney. In summary, our results showed that the subacute doses of crack cocaine used in this study had cytotoxic, and immunosuppressive effects in liver and kidney of rats, especially at 36 mg/kg dose. Since cellular death and inflammation participates in the multi-step process of chemical carcinogenesis, these data offer new insights into potential ways to understand the pathobiological mechanisms induced by crack cocaine in several tissues and organs.

AMPK in the gut-liver-brain axis and its influence on OP rats in an HSHF intake and WTD rat model.

Obesogenic diets (ODs) can affect AMPK activation in several sites as the colon, liver, and hypothalamus. OD intake can impair the hypothalamic AMPK regulation of energy homeostasis. Despite consuming ODs, not all subjects have the propensity to develop or progress to obesity. The obesity propensity is more associated with energy intake than expenditure dysregulations and may have a link with AMPK activity. While the effects of ODs are studied widely, few evaluate the short-term effects of terminating OD intake. Withdrawing from OD (WTD) is thought to improve or reverse the damages caused by the intake. Therefore, here we applied an OD intake and WTD protocol aiming to evaluate AMPK protein content and phosphorylation in the colon, liver, and hypothalamus and their relationship with obesity propensity. To this end, male Wistar rats (60 days) received control or high-sugar/high-fat (HSHF) OD for 30 days. Half of the animals were OD-withdrawn and fed the control diet for 48 h. After intake, we found a reduction in AMPK phosphorylation in the hypothalamus and colon, and after WTD, we found an increase in its hepatic and hypothalamic phosphorylation. The decrease in colon pAMPK/AMPK could be linked with hypothalamic pAMPK/AMPK after HSHF intake, while the increase in hepatic pAMPK/AMPK could have prevented the increase in hypothalamic pAMPK/AMPK. In the obesity-prone rats, we found higher levels of hypothalamic and colon pAMPK/AMPK despite the higher body mass gain. Our results highlight the relevance in multi-organ investigations and animal phenotype evaluation when studying the energy metabolism regulations.

Depression and obesity among females, are sex specificities considered?

This study aimed to systematically review the relationship of obesity-depression in the female sex. We carried out a systematic search (PubMed, MEDLINE, Embase) to quantify the articles (controlled trials and randomized controlled trials) regarding obesity and depression on a female population or a mixed sample. Successively, we established whether the sex specificities were studied by the authors and if they reported on collecting data regarding factors that may contribute to the evolution of obesity and depression and that could be responsible for the greater susceptibility of females to those conditions. After applying the inclusion and exclusion criteria, we found a total of 20 articles with a female sample and 54 articles with a mixed sample. More than half of all articles (51.35%, n = 38) evaluated the relationship between depression and obesity, but only 20 (27.03%) evaluated this relationship among females; still, 80% of those (n = 16) presented supporting results. However, few articles considered confounding factors related to female hormones (12.16%, n = 9) and none of the articles focused on factors responsible for the binomial obesity-depression in the female sex. The resulting articles also supported that depression (and related impairments) influencing obesity (and related impairments) is a two-way road. This systematic review supports the concurrency of obesity-depression in females but also shows how sex specificities are ultimately under-investigated. Female sex specificity is not being actively considered when studying the binomial obesity-depression, even within a female sample. Future studies should focus on trying to understand how the female sex and normal hormonal variations influence these conditions.

Palatable high-fat diet intake influences mnemonic and emotional aspects in female rats in an estrous cycle-dependent manner.

Worldwide, the excessive consumption of fat and/or sugar has increased considerably. Palatable high-fat diets (HFDs) lead to metabolic disturbances and obesity, and impact emotional and cognitive processes. Previous studies in rodent models suggested that HFDs often cause multiple behavioral alterations, such as learning and memory deficits, and anxiety-like behaviors. Different sexes imply different behavioral and cognitive abilities; yet, most of these studies dealt with male or ovariectomized rats. We evaluated HFD effects in female rats submitted to different behavioral tasks, considering the effects of endogenous hormonal variations throughout estrous cycle. Female Wistar rats in each phase of the estrous cycle using commercial chow (CC) or HFD for 32 days. During treatment, behavioral assessments using sucrose preference (SP), elevated plus-maze (EPM), open field (OF) and novel-object recognition (NOR). At the end of the behavioral tests, animals were euthanized, and performed an immunohistochemical analysis of the brains by brain-derived neurotrophic factor (BDNF) and tyrosine hydroxylase (TH). The main results demonstrated that (1) HFD-fed rats had higher body mass gain and food intake, without altering caloric intake, (2) rats in diestrus had lower sucrose intake, (3) females in metestrus and diestrus showed deficits in the novel-object recognition memory. Furthermore, TH-immunoreactivity decreased in the dorsal striatum and BDNF in the hippocampus in HFD-fed females. These results suggest that HFD alters neurochemical and metabolic aspects that may induce phase-dependent behavioral changes in female rats.

Withdrawing from obesogenic diets: benefits and barriers in the short- and long-term in rodent models.

There is accumulating evidence of dietary impact on several metabolic parameters. Unhealthy diets are estimated to be responsible for about 20% of the deaths worldwide. The recommendation is to improve the dietary pattern, aiming to prevent further harm. In this context, we reviewed the benefits and barriers of withdrawing from continuous obesogenic diet intake in the short- and long-term, which were found in rodent models. Although dietary modifications demand a re-establishment of the equilibrium, withdrawing was seen as a homeostatic insult and thus elicited several responses to protect the organism. In the short-term, withdrawal presented stressful and reward destimulating responses. The intake of obesogenic diets presented rewarding and stress destimulating responses. Whereas withdrawing in the long term ameliorated several biological functions and histopathologic features, it was not effective at reestablishing food intake and normalizing feeding behaviors or reward pathways. Altogether, terminating obesogenic diet intake does not immediately extinguish all negative consequences, and it even elicits brain behavioral and metabolic modifications. These modifications can hinder the maintenance of habits' change and prevent reaching the long-term benefits of diet improvement.

Prebiotic potencial of juçara berry on changes in gut bacteria and acetate of individuals with obesity.

PURPOSE: Whole plant foods can be fermentable by SCFA-producing bacteria and positively influence host adipose tissue development and obesity related-metabolic disorders, conferring a prebiotic role. Considering the juçara berry composition, rich in fiber and polyphenols, we hypothesized the probable prebiotic role of juçara in individuals with obesity. METHODS: It was a randomized double-blind placebo-controlled trial with 35 volunteers with obesity I and II of both sexes aged from 31 to 59 years, divided into juçara group (5 g lyophilized juçara) or placebo group (5 g of maltodextrin) for 6 weeks. Before and after supplementation, food intake and blood and stool samples were collected to evaluate serum LPS, SCFA, and microbial bacteria. RESULTS: Significant increase in fecal acetate (g = 0.809; p = 0.038) and in relative abundance of A. muciniphila, Bifidobacterium spp. and C. coccoides were observed in response to juçara supplementation (Δ% = 239.6%, 182.6%, and 214%, respectively), with a significant mediator role of Bifidobacterium spp. in high amounts of fecal acetate (z = 2.925; p = 0.003). To certify the prebiotic role of juçara, the averages were adjusted for total fiber intake; and there was no effect of the fiber intake on the SCFA nor on the intestinal bacteria. CONCLUSION: Juçara berry may haveprebiotic function, with emphasis on the bifidogenic effect, leading to increased excretion of acetate.

Effect of the intake of high or low glycemic index high carbohydrate-meals on athletes' sleep quality in pre-game nights.

This study investigated the effect of the intake of high (HGI) or low glycemic index (LGI) high-carbohydrate meals on athletes' sleep. Nine basketball adult male athletes were assessed during a championship and received high-carbohydrate meals (dinner and evening snack) with HGI or LGI. Quantitative and qualitative sleep variables were assessed: sleep latency (LAT), sleep efficiency (EFIC), Wake After Sleep Onset (WASO), sleep time through actigraphy and sleep diary. Dietary intake, satiety, sleepiness, glycemic response, salivary cortisol and melatonin were also assessed. On both days most athletes had LAT and WASO higher than recommendation, and nocturnal sleep time below the recommendations. There was no difference between sleep and hormonal parameters according to GI dietary manipulations; however, correlations were observed between sleep and diet. Daily energy intake had negative correlation with efficiency and nocturnal total sleep time, and a positive correlation with WASO, regardless of the GI nocturnal meals. No differences were observed in salivary cortisol and melatonin according to GI. The results suggest that food intake throughout the day seems to exert more influence on sleep parameters of basketball players than GI manipulation of evening meals on the pre-night game, but further studies are necessary to better understand this complex relationship.

Programming mediated by fatty acids affects uncoupling protein 1 (UCP-1) in brown adipose tissue.

Brown adipose tissue (BAT) has recently been given more attention for the part it plays in obesity. BAT can generate great amounts of heat through thermogenesis by the activation of uncoupling protein 1 (UCP-1), which can be regulated by many environmental factors such as diet. Moreover, the build-up of BAT relates to maternal nutritional changes during pregnancy and lactation. However, at present, there is a limited number of studies looking at maternal nutrition and BAT development, and it seems that the research trend in this field has been considerably declining since the 1980s. There is much to discover yet about the role of different fatty acids on the development of BAT and the activation of UCP-1 during the fetal and the postnatal periods of life. A better understanding of the impact of nutritional intervention on the epigenetic regulation of BAT could lead to new preventive care for metabolic diseases such as obesity. It is important to know in which circumstances lipids could programme BAT during pregnancy and lactation. The modification of maternal dietary fatty acids, amount and composition, during pregnancy and lactation might be a promising strategy for the prevention of obesity in the offspring and future generations.

Lipotoxicity: effects of dietary saturated and transfatty acids.

The ingestion of excessive amounts of saturated fatty acids (SFAs) and transfatty acids (TFAs) is considered to be a risk factor for cardiovascular diseases, insulin resistance, dyslipidemia, and obesity. The focus of this paper was to elucidate the influence of dietary SFA and TFA intake on the promotion of lipotoxicity to the liver and cardiovascular, endothelial, and gut microbiota systems, as well as on insulin resistance and endoplasmic reticulum stress. The saturated and transfatty acids favor a proinflammatory state leading to insulin resistance. These fatty acids can be involved in several inflammatory pathways, contributing to disease progression in chronic inflammation, autoimmunity, allergy, cancer, atherosclerosis, hypertension, and heart hypertrophy as well as other metabolic and degenerative diseases. As a consequence, lipotoxicity may occur in several target organs by direct effects, represented by inflammation pathways, and through indirect effects, including an important alteration in the gut microbiota associated with endotoxemia. Interactions between these pathways may perpetuate a feedback process that exacerbates an inflammatory state. The importance of lifestyle modification, including an improved diet, is recommended as a strategy for treatment of these diseases.

Effects of a diet enriched with polyunsaturated, saturated, or trans fatty acids on cytokine content in the liver, white adipose tissue, and skeletal muscle of adult mice.

This study analyzed the effect of diet enriched with 30% lipids on cytokines content in different tissues. Swiss male mice were distributed into four groups treated for 8 weeks with control (C, normolipidic diet); soybean oil (S); lard (L); and hydrogenated vegetable fat (H). We observed an increase in carcass fat in groups S and L, and the total amount of fatty deposits was only higher in group L compared with C group. The serum levels of free fatty acids were lower in the L group, and insulin, adiponectin, lipid profile, and glucose levels were similar among the groups. IL-10 was lower in group L in mesenteric and retroperitoneal adipose tissues. H reduced IL-10 only in retroperitoneal adipose tissue. There was an increase in IL-6 in the gastrocnemius muscle of the L group, and a positive correlation between TNF-α and IL-10 was observed in the livers of groups C, L, and H and in the muscles of all groups studied. The results suggested relationships between the quantity and quality of lipids ingested with adiposity, the concentration of free fatty acids, and cytokine production in white adipose tissue, gastrocnemius muscle, and liver.

ALZHEIMER'S DISEASE AND ITS RELATIONSHIP WITH THE MICROBIOTA-GUT-BRAIN AXIS.

BACKGROUND: Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease, characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain. Several pathways enable bidirectional communication between the central nervous system (CNS), the intestine and its microbiota, constituting the microbiota-gut-brain axis. OBJECTIVE: Review the pathophysiology of AD, relate it to the microbiota-gut-brain axis and discuss the possibility of using probiotics in the treatment and/or prevention of this disease. METHODS: Search of articles from the PubMed database published in the last 5 years (2017 to 2022) structure the narrative review. RESULTS: The composition of the gut microbiota influences the CNS, resulting in changes in host behavior and may be related to the development of neurodegenerative diseases. Some metabolites produced by the intestinal microbiota, such as trimethylamine N-oxide (TMAO), may be involved in the pathogenesis of AD, while other compounds produced by the microbiota during the fermentation of food in the intestine, such as D-glutamate and fatty acids short chain, are beneficial in cognitive function. The consumption of live microorganisms beneficial to health, known as probiotics, has been tested in laboratory animals and humans to evaluate the effect on AD. CONCLUSION: Although there are few clinical trials evaluating the effect of probiotic consumption in humans with AD, the results to date indicate a beneficial contribution of the use of probiotics in this disease.

Proanthocyanidins in grape seeds and their role in gut microbiota-white adipose tissue axis.

Several factors can impact the gut microbiota, affecting host metabolism and immunity. It implies intestinal barrier disruption and translocation of gut microbiota metabolites to the bloodstream, such as lipopolysaccharides (LPS). LPS is an endotoxin from gram-negative gut bacteria that trigger the activation of the Toll-like receptor-4 (TLR-4) inflammatory pathway and can modulate white adipose tissue (WAT) metabolism. Dietary components, including diets rich in fiber and polyphenols, contribute to intestinal environment homeostasis. Grape seed proanthocyanidins extract (GSPE) may improve intestinal permeability and microbial diversity and increase short-chain fatty acids production. Furthermore, GSPE has been involved in LPS reduction, down-regulating the TLR-4 pathway, decreasing the WAT metainflammatory profile, and preventing adipocyte hypertrophy. Studies have pointed out strategies to promote health and control obesity by modulating the gut microbiota environment. Therefore, this review aims to summarize the potential effects of GSPE on the gut microbiota-white adipose tissue axis against obesity.

Hippocampal BDNF mediated anxiety-like behaviours induced by obesogenic diet withdrawal.

Obesogenic diets (ODs) consumption is associated with anxiety-like behaviour and negative changes in hippocampal BDNF. At the same time, interrupting OD intake, OD withdrawal (WTD), can bring health benefits, but previous studies reported the development of anxiety-like behaviours. The present work aimed to assess the relationship between anxiety-like behaviour with hippocampal BDNF in a WTD rodent model. Male Wistar rats (60d old) were fed a high-sugar/high-fat (HSHF) diet for 30d (n = 32), and half of them were transitioned to a control diet for 48 h (n = 16) afterwards. The control group (n = 16) was fed a control diet across the whole experiment. Besides increasing anxiety-like behaviours and lowering sociability, the WTD led to an increase in BDNF in the dentate gyrus and the CA1 of the hippocampus. It also decreased locomotor activity in both OF and EPM, however, they did not significantly interfere with the other behavioural parameters analysed. Western blotting analysis revealed that the increase in BDNF likely occurred in the mature forms (14 kD monomer and 28 kD dimer). The mediation models analyses suggested that the effect of WTD on anxiety-like behaviour was driven by hippocampal BDNF, this mediation of effect was region-dependent. Our results also suggested that mature BDNF forms (14 kD and 28 kD) were responsible. The present work brought light to a possible new role for mature BDNF, although it is generally associated with beneficial features, it can also be part of the genesis of anxiety-like behaviours and sociability aspects on WTD models.

Anthocyanins ameliorate obesity-associated metainflammation: Preclinical and clinical evidence.

The growing rates of obesity worldwide call for intervention strategies to help control the pathophysiological consequences of weight gain. The use of natural foods and bioactive compounds has been suggested as such a strategy because of their recognized antioxidant and anti-inflammatory properties. For example, polyphenols, especially anthocyanins, are candidates for managing obesity and its related metabolic disorders. Obesity is well known for the presence of metainflammation, which has been labeled as an inflammatory activation that leads to a variety of metabolic disorders, usually related to increased oxidative stress. Considering this, anthocyanins may be promising natural compounds able to modulate several intracellular mechanisms, mitigating oxidative stress and metainflammation. A wide variety of foods and extracts rich in anthocyanins have become the focus of research in the field of obesity. Here, we bring together the current knowledge regarding the use of anthocyanins as an intervention tested in vitro, in vivo, and in clinical trials to modulate metainflammation. Most recent research applies a wide variety of extracts and natural sources of anthocyanins, in diverse experimental models, which represents a limitation of the research field. However, the literature is sufficiently consistent to establish that the in-depth molecular analysis of gut microbiota, insulin signaling, TLR4-triggered inflammation, and oxidative stress pathways reveals their modulation by anthocyanins. These targets are interconnected at the cellular level and interact with one another, leading to obesity-associated metainflammation. Thus, the positive findings with anthocyanins observed in preclinical models might directly relate to the positive outcomes in clinical studies. In summary and based on the entirety of the relevant literature, anthocyanins can mitigate obesity-related perturbations in gut microbiota, insulin resistance, oxidative stress and inflammation and therefore may contribute as a therapeutic tool in people living with obesity.