Dietary fat strongly affects human health by modulating gut microbiota composition and low-grade systemic inflammation. High-fat diets have been implicated in reduced gut microbiota richness, increased Firmicutes to Bacteroidetes ratio, and several changes at family, genus and species levels. Saturated (SFA), monounsaturated (MUFA), polyunsaturated (PUFA) and conjugated linolenic fatty acids share important pathways of immune system activation/inhibition with gut microbes, modulating obesogenic and proinflammatory profiles. Mechanisms that link dietary fat, gut microbiota and obesity are mediated by increased intestinal permeability, systemic endotoxemia, and the activity of the endocannabinoid system. Although the probiotic therapy could be a complementary strategy to improve gut microbiota composition, it did not show permanent effects to treat fat-induced dysbiosis. Based upon evidence to date, we believe that high-fat diets and SFA consumption should be avoided, and MUFA and omega-3 PUFA intake should be encouraged in order to regulate gut microbiota and inflammation, promoting body weight/fat control.

CONTEXT AND OBJECTIVE: Diet is an important modifiable factor involved in obesity-induced inflammation. We reviewed clinical trials that assessed the effect of consumption of different fatty acids on the expression of inflammation-related genes, such as cytokines, adipokines, chemokines and transcription factors. DESIGN AND SETTING: Narrative review study conducted at a research center. METHODS: This was a review on the effect of fat intake on inflammatory gene expression in humans. RESULTS: Consumption of saturated fatty acids (SFAs) was related to postprandial upregulation of genes associated with pro-inflammatory pathways in peripheral blood mononuclear cells (PBMCs), in comparison with monounsaturated fatty acid (MUFA) or polyunsaturated fatty acid (PUFA) intake. In addition, acute intake of a high-SFA meal also induced a postprandial pro-inflammatory response for several inflammatory genes in subcutaneous adipose tissue. Both high-MUFA and high-PUFA diets showed anti-inflammatory profiles, or at least a less pronounced pro-inflammatory response than did SFA consumption. However, the results concerning the best substitute for SFAs were divergent because of the large variability in doses of MUFA (20% to 72% of energy intake) and n3 PUFA (0.4 g to 23.7% of energy intake) used in interventions. CONCLUSIONS: The lipid profile of the diet can modulate the genes relating to postprandial and long-term inflammation in PBMCs and adipose tissue. Identifying the optimal fat profile for inflammatory control may be a promising approach for treating chronic diseases such as obesity.

There is a growing mortality related to co-morbidities associated with diabetes mellitus. Intake of polyunsaturated fatty acids (PUFA) has been associated with low cardiometabolic risk and reduction of inflammatory process. The objective of this paper is to review the impact of PUFA intake on glycemic control in diabetic patients as well as to elucidate the possible mechanisms involved. Medline/PubMed electronic database was searched to identify studies published within last five years regarding the effect of PUFA intake on glucose metabolism in type 2 diabetics. The search terms used were “polyunsaturated fatty acid(s),” “PUFA,” and “diabetes.” We included only interventional studies that assessed the effects of PUFA intake on glucose metabolism – fasting glucose, serum insulin, HbA1c, and HOMA-IR assessment– in type 2 diabetics. Initially, 48 articles were identified, of which one was not available and 41 did not match the inclusion criteria. Within the selected studies, three articles showed an improvement in fasting blood glucose, two showed an increase in fasting glycemia, and there was no effect of intervention in one article only. Based on the analyzed clinical interventional studies, supplementation of 0.42–5.2-g PUFA/day for at least eight weeks may become an alternative treatment for type 2 diabetes mellitus, particularly in Asian subjects.

The metabolic effects of cranberry and blueberry consumption on glycemic control have been evaluated in vitro and in animal models as well as in human studies, although findings have not been systematically reviewed yet. Therefore, a systematic review was carried out of relevant randomized clinical trials (RCTs) in order to assess the effect of berries (blueberry and cranberry) consumption on type 2 diabetes (T2DM) glycemic control. Some evidences were also discussed on the anti-diabetic mechanisms exerted by berries polyphenols. Studies were identified by searching electronic databases: LILACS, PubMed/MEDLINE, Scopus, The Cochrane Library and Web of Science. Three authors independently searched and extracted RCTs in which the effect of berries (cranberry or blueberry) consumption on T2DM glycemic control was assessed. A total of 7 RCTs, involving 270 adults with type 2 diabetes were included. Despite the heterogeneity of the administration forms (in natura, dried, extract, preparations – juice), dosage, duration of the intervention and type of population of the studies involving these two berries some studies highlight the potential benefit of berries, especially of blueberry, on glucose metabolism in T2DM subjects. Daily cranberry juice (240 mL) consumption for 12 weeks and blueberry extract or powder supplementation (9.1 to 9.8 mg of anthocyanins, respectively) for 8 to 12 weeks showed a beneficial effect on glucose control in T2DM subjects. Those results indicate a promising use of these berries in T2DM management; although more studies are required to better understand the mechanisms involved.

We aimed to evaluate the postprandial secretion of inflammatory markers induced by SFA or MUFA high-fat meal consumption and whether orange juice intake could modulate this induction. This study included 55 healthy women (aged 20 to 40 years): 33 participants received an SFA high-fat meal (≈1000 kcal, 37.6% of energy intake (E) from SFA) and 22 participants received an MUFA high-fat meal (≈1000 kcal, 56.3% E from MUFA). Both interventions were accompanied by 500 ml of orange juice (test) or water (control). The plasma concentrations of inflammatory cytokines (IL-2, IL-4, IL-6, IL-10, IL-17A, IFN-γ, and TNF-α) and CRP were determined before (fasting) and 2, 3 and 5 hours after the test meal intake. The SFA high-fat meal induced a significant increase in AUC values (for TNF-α, IL-12, IL-10, IL-6 and IL-2 adjusted for baseline concentrations) in comparison with MUFA high-fat meal intervention. The results were independent of the drink which accompanied the meal (water or orange juice). Both IL-4 and IL-17A AUC values were significantly increased after an SFA high-fat meal intake, accompanied by water, but not by orange juice. In addition, these values were higher in relation to MUFA high-fat meal interventions. Also, IL-17A significantly increased at 3 h after an SFA high-fat meal intake accompanied by water, but not by orange juice. Overall, our conclusions indicate an anti-inflammatory effect of MUFA compared to SFA high-fat meal intake, while orange juice intake was able to mitigate the subclinical increase of postprandial inflammation, induced by SFA high-fat meal consumption, for a particular biomarker (IL-17A).