Recent studies have suggested that excessive intake of dietary fat is associated with obesity. Some obese subjects have been reported to exhibit high thresholds for the gustatory detection of lipids via lipid receptors, such as cluster of differentiation 36 (CD36). We studied lingual detection thresholds for emulsions containing oleic acid in obese Tunisian women (n 203) using a three-alternative forced choice (3-AFC) method. Genotyping of the TNF-a (rs1800629), IL-6 (rs1800795) and CD36 (rs1761667) genes was performed to associate with lipid taste perception thresholds. The CD36 genotype distribution was as follows: GG (n 42), AG (n 102) and AA (n 59). Women with the CD36 GG genotype exhibited oral detection thresholds for oleic acid that were more than three times lower than those with the CD36 AA genotype. The present study confirms a high threshold of gustatory fat detection in obese women with the CD36 AA genotype, but there is no significant association with the IL-6 and TNF-a gene polymorphisms.Key words: Obesity: Lipids: Taste: Genes As the obesity epidemic continues, more subjects are getting fatter and are therefore at increased risk for metabolic complications, hypertension and cancer-related mortality (1,2) . The aetiology of obesity is multifactorial, and genetic inheritance and behavioural/environmental causes are considered to be the main factors (3) . Dietary fat is considered palatable to humans, and several factors, including its olfactory, visual and textural properties, have been proposed as playing a key role in the attractiveness of fat (4) . Humans and rodents can detect long-chain fatty acids in their diets as gustatory cues (4 -9) . Some recent studies have shown that obese subjects exhibit a high preference for dietary lipids as compared to lean subjects (10,11) , which suggests that inappropriate lipid perception might influence obesity risk by impacting feeding behaviour. In fact, obesity is associated with a low sensitivity to the oro-sensorial detection of fat (10,11) .Lingual cluster of differentiation 36 (CD36), like G proteincoupled receptor 120 (GPR120) and G protein-coupled receptor 40 (GPR40), has been shown to act as a lipid receptor that is involved in a spontaneous preference for fat (6,12 -15) . The lingual lipid receptors bind to long-chain fatty acids, which are released by lingual lipases in the buccal cavity (12 -15) . We performed the present study on CD36 SNP because CD36 is a high-affinity receptor, whereas GPR120 and GPR40 are low-affinity receptors. In addition, GPR40 could not be detected on human lingual epithelium (16) . Moreover, Sclafani et al. (17) have shown that CD36 is directly involved in early fat detection, whereas GPR120 plays a role in the post-ingestive regulation of fat preference (18) .Recent studies have shown that CD36 protein expression is influenced by CD36 gene polymorphism, and it is related to the detection threshold of dietary lipids in obese subjects (19) . Keller et al. (20) reported that obese subjects with the CD36 AA geno...

Abstract. Gestational diabetes mellitus (GDM) is pathology of glucose intolerance during pregnancy. It is influenced by maternal hyperglycemia and insulinemia through placental circulation. The study was undertaken to investigate the implication of pro-inflammatory factors in the placenta of GDM women. Thirty GDM women have delivered macrosomic babies, and 30 healthy age-matched pregnant women have delivered non macrosomic babies, were recruited in the study. The mRNAs encoding for IL-6, TLR4, TGF-β, CD68, CD14, EMR-1, CCL2, TCR-α, T-bet, GATA-3, leptin and adiponectin were quantified in placental samples by using RT-qPCR. The mRNA expression of the pro-inflammatory factors, i.e., IL-6, TLR4 and TGF-β, was increased in GDM placenta. The mRNA expression of markers of infiltration of macrophage, i.e., CD68, CD14 and EMR-1, was higher in the GDM placenta than the control placenta. The expression of mRNA of TCR-α, an indicator of T-cell infiltration, was significantly higher in the GDM placenta. Interestingly, the expression of mRNA of GATA-3, an indicator of Th2 phenotype differentiation, was unregulated in the GDM placenta. Leptin and adiponectin mRNAs were also significantly increased in the placenta of the GDM group. Our results revealed that there is an increase of inflammation in the GDM placenta which might be involved, in part, in the pathogenesis of macrosomia.

BackgroundTo evaluate whether abnormal endothelial function, a common finding in gestational diabetes mellitus (GDM) pregnancies, can be explained by inflammatory cytokines.MethodsForearm skin blood flow (FSBF), into response to acetylcholine (Ach) (endothelium-dependent vasodilatation), were measured in 24 pregnant control subjects and 28 gestational diabetes mellitus (GDM) women, in the third trimester of gestation. A fasting glycemic and lipidic panel was obtained, and inflammatory cytokines (TNF-α and IL-6) and adiponectin were also determined.ResultsFSBF is significantly reduced in GDM group compared with control subjects (344.59 ± 57.791 vs.176.38 ± 108.52, P < 0.05). Among all subjects, FSBF showed a strong negative correlation with TNF-α and IL-6 (r = −0.426, P < 0.0001 and r = −0.564, P < 0.0001, respectively) and positive correlation with adiponectin (r = 0.468, P < 0.0001).ConclusionsEndothelial function, an early marker of macrovascular disease, is present in non-obese pregnancies complicated by GDM. This alteration seems to be directly related to inflammatory status, which may represent a patho-physiological link between GDM and type 2 diabetes and, later on, metabolic syndrome.

The purpose of this study was to determine the effect of different modalities of individualized active recovery on blood lactate disappearance after supramaximal exercise in subjects with different levels of aerobic fitness. Fourteen healthy subjects (7 trained and 7 untrained subjects mean age 20 +/- 1.5 and 19.5 +/- 1.5, respectively) participated in this study. They performed three supramaximal intermittent exercises at 60 % of the time to exhaustion at 120 % of the maximum aerobic power (MAP) with 5-min recovery periods (2 x 5 min). The third exercise was followed by 20 min of recovery. The effects of four types of recovery were compared in trained and untrained subjects: passive recovery (PR), an active recovery at an intensity corresponding to the first anaerobic ventilatory threshold minus 20 % (VT1), an active recovery at an intensity corresponding to the second anaerobic ventilatory threshold minus 20 % (VT2) and a combined active recovery (CR) which consisted of 7 min at VT2 followed by 13 min at VT1. Blood lactate levels were measured at rest and during the recovery periods. Peak blood lactate after supramaximal exercise was observed significantly earlier with VT2 and CR (4th min) than VT1 and PR (7th min) in trained and in untrained subjects. Combined active recovery (CR) showed a significantly faster lactate disappearance than did PR, VT1, or VT2 from the 7th min of recovery in trained subjects (p < 0.05) and at the 20th min in untrained subjects (p < 0.05). CR and VT2 conditions showed earlier peak blood lactate (4th min) than PR or VT1 (7th min). Blood lactate disappearance was faster in trained than untrained subjects during combined active recovery. This result suggests that the level of physical fitness plays an important role mainly in the pattern of blood lactate decrease during combined active recovery.

Th (T helper) cells are differentiated into either Th1 or Th2 phenotype. It is generally considered that Th1 phenotype is proinflammatory, whereas Th2 phenotype exerts anti-inflammatory or protective effects. Gestational diabetes mellitus (GDM) has been associated with a decreased Th1 phenotype, whereas macrosomia is marked with high expression of Th1 cytokines. Besides, these two pathological situations are marked with high concentrations of inflammatory mediators like tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), known to play a pivotal role in insulin resistance. Dietary n-3 polyunsaturated fatty acids (n-3 PUFAs) may exert a beneficial effect by shifting Th1/Th2 balance to a Th2 phenotype and increasing insulin sensitivity. In this paper, we shed light on the role of T-cell malfunction that leads to an inflammatory and pathophysiological state, related to insulin resistance in GDM and macrosomia. We will also discuss the nutritional management of these pathologies by dietary n-3 polyunsaturated fatty acids (PUFAs).