Daniela Mayumi Usuda Prado Rocha

Saturated fatty acids trigger TLR4-mediated inflammatory response.

Toll-like receptors (TLR) mediate infection-induced inflammation and sterile inflammation by endogenous molecules. Among the TLR family, TLR4 is the best understood. However, while its downstream signaling pathways have been well defined, not all ligands of TLR4 are currently known. Current evidence suggests that saturated fatty acids (SFA) act as non-microbial TLR4 agonists, and trigger its inflammatory response. Thus, our present review provides a new perspective on the potential mechanism by which SFAs could modulate TLR4-induced inflammatory responses: (1) SFAs can be recognized by CD14-TLR4-MD2 complex and trigger inflammatory pathways, similar to lipopolysaccharide (LPS). (2) SFAs lead to modification of gut microbiota with an overproduction of LPS after a high-fat intake, enhancing this natural TLR4 ligand. (3) In addition, this metabolic endotoxemia leads to an oxidative stress thereby producing atherogenic lipids - oxLDL and oxidized phospholipids - which trigger CD36-TLR4-TLR6 inflammatory response. (4) Also, the high SFA consumption increases the lipemia and the mmLDL and oxLDL formation through oxidative modifications of LDL. The mmLDL, unlike oxLDL, is involved in activation of the CD14-TLR4-MD2 inflammatory pathway. Those molecules can induce TLR4 inflammatory response by MyD88-dependent and/or MyD88-independent pathways that, in turn, promotes the expression of proinflammatory transcript factors such as factor nuclear kappa B (NF-κB), which plays a crucial role in the induction of inflammatory mediators (cytokines, chemokines, or costimulatory molecules) implicated in the development and progression of many chronic diseases.

Polyunsaturated fatty acids and type 2 diabetes: Impact on the glycemic control mechanism

ABSTRACT 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.

Impact of dietary fat on gut microbiota and low-grade systemic inflammation: mechanisms and clinical implications on obesity.

Abstract 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.

The role of dietary fatty acid intake in inflammatory gene expression: a critical review

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.

Effects of blueberry and cranberry consumption on type 2 diabetes glycemic control: A systematic review

ABSTRACT 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.

Postprandial Lipid Response to High-Saturated and High-Monounsaturated Fat Meals in Normal-Weight or Overweight Women

ABSTRACT Purpose: We evaluated postprandial response of the lipid metabolism markers after the intake of a high-saturated fat (HSM) or high-monounsaturated fat meal (HMM). Methods: A randomized, controlled and acute intervention study included 63 women (age 26.9 ± 6.1 years): 35 normal weight (NW) and 28 overweight (OW) (total body fat [TBF] 24.7 ± 3.9% and 36.6 ± 3.9%, respectively). After 12 hours of fasting, each subject was given one of the two test meals standardized, including 2 muffins and water (HSM, 42.1% of saturated fat acid, or HMM, 34.5% of monounsaturated fat acid). Plasma fatty acid profile and concentrations of apolipoproteins A1 and B100, complement C3, and triacylglycerols were analyzed during fasting and at 2, 3, and 5 postprandial hours. Results: Among the markers studied, the triacylglycerol (TAG) and complement C3 were significantly higher in the OW group, compared to NW. The increment in the C3 concentration was higher after HSM intake, compared with HMM (iAUC = 4365.5 ± 5477.4 vs. 1215.2 ± 882.4; p = 0.006), with no differences between groups. After 5 hours postprandial, plasma oleic acid values remained high compared with the fasting value in the NW group, but not in the OW group (26.0 ± 4.2 vs 23.7 ± 3.9%; p < 0.001). Women with high percentage of total plasma saturated fatty acids (SFA) at the beginning of the intervention had higher incremental area under the curve (iAUC) for the palmitic, stearic, and total fatty acids (p < 0.005). Those women with a high percentage of monounsaturated fatty acids (MUFA) showed lower iAUC values for the same fatty acid profile (p < 0.005). Conclusion: This study demonstrated the effect of the HSM on postprandial increment of C3 concentration, suggesting another mechanism for saturated fat metabolism. The postprandial response to HSM appears to be the mediated by baseline lipid profile of the individuals, while the response to HMM was correlated to the weight status.

Acute Effect of Coconut Oil Consumption does not Affect Postprandial Human Cytokines in Healthy Overweight Women

The coconut oil is popularly recognized for its anti-inflammatory properties, but research has shown conflicting results. Thus, our aim was to assess the postprandial inflammatory response of moderate coconut oil intake. We evaluated the acute consumption of a breakfast, offered in a single day, containing 25 mL of coconut oil (test) or 25 mL of olive oil (control)on postprandial serum inflammatory cytokines (IL-2, IL-4, IL-6, IL-10, IL-17A, IFN-γ and TNF) in healthy overweight women. No change was observed in relation to the effect of fatty meals, the time and the interaction of both factors (meal x time). Thus, despite being a saturated fat source, coconut oil consumption did not promote an inflammatory response. Further studies are needed considering a larger intervention period to check long-term effect. *Corresponding author: Daniela Mayumi Usuda Prado Rocha, Av PH Rolfs s/n, Federal University of Vicosa, Department of Nutrition and Health, Viçosa, Minas Gerais, CEP: 36570-900, Brazil, Tel: +55 31 3899 3388; E-mail: mayumi.dani@gmail.com Received Date: October 08, 2016 Accepted Date: October 22, 2016 Published Date: October 28, 2016

Queijo "Petit suisse" de kefir: uma alternativa de sobremesa com microorganismos de ação probiótica

The effect of replacing shortening and sugar on the physical and chemical properties of mangaba ice cream and its acceptability were evaluated. Ice cream fo...