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Impact of Dietary and Exercise Interventions on Brain Insulin Action and Brain Function
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Specific dietary factors, which are consistently negatively associated with T2DM risk, are overnutrition/obesity, whole grain products and insoluble fiber (16, 17), coffee (with or without caffeine) (18), legumes, and moderate amounts of alcohol. Sugars and other high-glycemic index (GI) foods, artificial sweeteners, and red meat are linked to a higher T2DM risk (19–21). Fish, tea, and dairy have not been consistently shown to affect diabetes risk (22, 23). Some genes within the T2DM risk profile show a nutrigenetic association with either T2DM incidence or continuous parameters, e.g. ACE, FABP2, TCF7L2 (24–26). There are also still inconclusive nutrigenomic associations between fiber intake, diabetes risk or glycemic outcomes, and genes, related to incretin secretion and NAFLD (27–30). High animal protein intake is considered a diabetes risk factor, while moderate intake of plant protein is seen as protective (31). Saturated, cis-monosaturated, and cis-polyunsaturated fatty acids show no epidemiological association with T2DM. Non-ruminant trans fats are classified as diabetogenic, while animal-based trans-fatty acids are not (32).
Noninsulin-Dependent Animal Models of Diabetes Mellitus
Published in John H. McNeill, Experimental Models of Diabetes, 2018
Christopher H. S. McIntosh, Raymond A. Pederson
Adipocyte fatty acid–binding protein 2 (FABP2) binds to fatty acids such as oleic acid and retinoic acid, although its function is not entirely clear. Linkage analysis indicated that a gene on human chromosome 4q(26) close to the FABP2 gene (aP2) is associated with NIDDM in Pima indians.380 Mice with a null mutation in aP2 were metabolically and developmentally normal.381 However, the knockout (aP2-−/−) animals developed dietary obesity but, unlike aP2+/+ mice, they did not become either insulin resistant or diabetic. Interestingly, obese aP2−/− mice did not express TNF-α in adipose tissue. These authors therefore speculated that FABP2 links obesity and insulin resistance by coupling fatty acid metabolism to TNF-α expression.
Association between the FABP2 Ala54Thr and CRP+1059C/G polymorphisms and small dense LDL level in patients with atherosclerosis: a case–control study
Published in Archives of Physiology and Biochemistry, 2023
Banafsheh Yalameha, Mehdi Birjandi, Negar Nouryazdan, Hamid Nasri, Gholamreza Shahsavari
It has been indicated that abnormality in the regulation of lipid metabolism and inflammatory responses might result in the occurrence of atherosclerosis. Moreover, previous studies have revealed the positive relationship between increased plasma lipid levels and the risk of cardiovascular events (Aulchenko et al. 2009, Shahsavari et al. 2017). Fatty acid-binding protein 2 (FABP2) is an intracellular protein with a molecular weight of 15 kDa which is expressed in small intestinal enterocytes. FABP2 has significant roles in various pathways of lipids transfusion and absorption, including the absorption of saturated and unsaturated long-chain fatty acids and the regulation of enzymes involved in lipid metabolism (Besnard et al. 1996, Van Nieuwenhoven et al. 1996). The gene encoding FABP2 is located on the long arm of chromosome 4 in the 4q28-q31 region and contains four exons and three introns (Smathers and Petersen 2011). In the coding sequence of the FABP2 gene, a mutation in codon 54 has been identified that involves the substitution of alanine by threonine (Tavridou et al.2009). Previous evidences have revealed that the Ala54Thr polymorphism corresponds to increased triglyceride levels, obesity, type 2 diabetes and insulin resistance. Ala54Thr polymorphism might alter the transportation of dietary fatty acids and subsequently elevate saturated fatty acids level, endothelial dysfunction and cardiovascular diseases (Levy et al.2001, Alharbi et al.2014).
Silicon dioxide nanoparticle exposure affects small intestine function in an in vitro model
Published in Nanotoxicology, 2018
Zhongyuan Guo, Nicole J. Martucci, Yizhong Liu, Eusoo Yoo, Elad Tako, Gretchen J. Mahler
The FABP family of fatty acid binding proteins mediates more than 95% of lipid digestion products targeting and shuttling to specific metabolic sits, and L-FABP (FABP1) and I-FABP (FABP2) are located in the absorptive intestinal villus cell (Tso et al. 1981; Agellon, Toth, and Thomson 2002; Boord, Fazio, and Linton 2002; Derikx et al. 2007; Mansbach and Gorelick 2007; Abumrad and Davidson 2012; Gajda and Storch 2015). Chronic SiO2 NP exposure significantly increased gene expression of FABP2, and the expression of FABP1 was significantly decreased by all chronic doses of SiO2 (Table 2). I-FABP is an early marker for enterocyte cell death. It is present in the plasma of healthy individuals in small amounts, but level rises rapidly after episodes of acute intestinal ischemia and inflammation (Derikx et al. 2007). FABP2 gene expression upregulation following chronic exposure to SiO2 NP may be due to pro-inflammatory signaling. Fatty acid uptake was not significantly changed by acute SiO2 exposure, but low, chronic NP exposure significantly decreased fatty acid uptake (Figure 4). IAP has been shown to be a negative regulator of intestinal fat absorption (Lallès 2010), and IAP levels were elevated following medium acute and medium and high chronic SiO2 NP exposures.