Excessive Lipid Intake Research Articles

Analysis of the mechanism of resistance to enzymatic hydrolysis of RS-5 resistant starch

RS-5 refers to the resistant starch formed by complexation of starch molecules with other molecules. In this study, the molecular mechanism of RS-5 was analysed. First, it was found, when α-amylase acted on the starch-lipid complexes, the glucose residues involved in complexation cannot be hydrolyzed by α-amylase, while the glucose residues not directly involved in complexation can be hydrolyzed. Second, lipid molecules are not necessary for the formation of RS-5 and can be replaced with small peptides or decanal molecules. Considering the multiple health hazards that may result from excessive lipid intake, small peptides composed of essential amino acids may be more desirable materials for RS-5 preparation. Third, starch-lipid complexes had strong interactions with α-amylase, which provides evidence in support of the sliding continuum hydrolysis hypothesis of α-amylase. These results revealed the mechanism of RS-5 at the molecular level, which provides a reference for the production and research of RS-5.

CD36: The Bridge between Lipids and Tumors.

It has been found that the development of some cancers can be attributed to obesity, which is associated with the excessive intake of lipids. Cancer cells undergo metabolic reprogramming, shifting from utilizing glucose to fatty acids (FAs) for energy. CD36, a lipid transporter, is highly expressed in certain kinds of cancer cells. High expressions of CD36 in tumor cells triggers FA uptake and lipid accumulation, promoting rapid tumor growth and initiating metastasis. Meanwhile, immune cells in the tumor microenvironment overexpress CD36 and undergo metabolic reprogramming. CD36-mediated FA uptake leads to lipid accumulation and has immunosuppressive effects. This paper reviews the types of FAs associated with cancer, high expressions of CD36 that promote cancer development and progression, effects of CD36 on different immune cells in the tumor microenvironment, and the current status of CD36 as a therapeutic target for the treatment of tumors with high CD36 expression.

Фактори ризику розвитку функціональних гастроінтестинальних розладів у дітей

The purpose is to analyze the risk factors for functional gastrointestinal disorders (FGID) in children, which will prevent their development and optimize therapy. The article presents an analysis of the literature on risk factors for the most common disorders: functional dyspepsia and irritable bowel syndrome. Among all potential predictors of FGID, chronic psychological stress is the most significant. The main triggers for its occurrence are sleep disturbance, excessive mental stress, dissatisfaction with family relationships with friends and parents, abuse of gadgets, smartphones, etc. Among the predictors of FGID, scientists consider malnutrition, starting from an early age, namely artificial feeding, to be no less important. In older adults, excessive lipid intake, adherence to FODMAPs diets, and consumption of ultra-processed foods are considered risk factors for FGID. In addition, a violation of the diet, the use of cold dishes also contribute to the occurrence of dysfunctions of the gastrointestinal tract. An important aspect of studying risk factors for FGID is the level of physical activity of children, as well as their nutritional status. Functional gastrointestinal disorders are conditions characterized by recurrent abdominal pain not explained by structural or biochemical disorders. The interest in functional pathology is quite justified and understandable: despite the fact that functional diseases of the gastrointestinal tract do not pose an immediate threat to the patient's life, they significantly reduce its quality: they affect all segments of society, regardless of socioeconomic status, gender or race, violate the microclimate in the family, which leads to anxiety of the child and parents, form long-term consequences in the future, contribute to a long diagnostic search, repeated consultations, unjustified appointments and expenses. Such a subject of discussion cannot remain without research interest due to the fact that the identification of the main risk factors for FGID will prevent their development, improve the quality of life, reduce the time and cost of examining a patient, and optimize therapy. No conflict of interests was declared by the authors.

Lipid-Lowering Effects of Inonotus obliquus Polysaccharide In Vivo and In Vitro.

Excessive lipid intake will cause hyperlipidemia, fatty liver metabolism disease, and endanger people’s health. Edible fungus polysaccharide is a natural active substance for lipid lowering. In this study, the HepG2 cell model induced by oleic acid and mice model induced by a high-fat diet was established. The lipid-lowering effects of Inonotus obliquus polysaccharide (IOP) was investigated in vivo and in vitro. Glucose (251.33 mg/g), rhamnose (11.53 mg/g), ribose (5.10 mg/g), glucuronic acid (6.30 mg/g), and galacturonic acid (2.95 mg/g) are present in IOP, at a ratio of 85.2:3.91:1.73:2.14:1. The molecular weight of IOP is 42.28 kDa. Treatment with 60 mg/L of IOP showed a significant lipid-lowering effect in HepG2 cells compared with the oleic acid-treated group. In the oil red O-stained images, the red fat droplets in the IOP-treated groups were significantly reduced. TC and TG levels of IOP-treated groups decreased. IOP can alleviate the lipid deposition in the mice liver due to high-fat diet, and significantly reduce their serum TC, TG, and LDL-C contents. IOP could activate AMPK but decrease the SREBP-1C, FAS, and ACC protein expression related to adipose synthesis in mice. IOP has a certain potential for lipid-lowering effects both in vivo and in vitro.

Hepatoprotective and Anti-Obesity Properties of Sardine By-Product Oil in Rats Fed a High-Fat Diet.

Excess lipid intake can trigger liver lipid accumulation and oxidative responses, which can lead to metabolic disturbances and contribute to hepatic steatosis and obesity and increase the risk of cardiovascular disease. Production of fish oil rich in omega-3 is a good opportunity for valorizing fish by-products in the therapeutic field. In this study, we explored the effects of oil from Sardina pilchardus by-products on cardiometabolic and oxidative disorders caused by toxic effects of excess lipids in obese rats. Three groups of obese rats received either 20% sardine by-product oil (SBy-Ob-HS; experimental group), 20% fillet oil (SF-Ob-HS; positive control group), or a high-fat diet (Ob-HS). Normal weight rats received a standard diet (normal). There was a significant decrease in serum total cholesterol (TC), triacylglycerols (TG), and insulin concentrations in the SBy-Ob-HS group compared with the SF-Ob-HS group. Compared with the Ob-HS group, TC and TG, glycemia, glycosylated hemoglobin, and insulinemia were decreased in the SBy-Ob-HS (more notably) and SF-Ob-HS groups. Furthermore, hepatic lipids, low density lipoprotein-cholesterol (C), the non-esterified cholesterol/phos-pholipids ratio, serum transaminases activities and lipid peroxidation were lower and serum high density lipoproteins-C were higher in the SBy-Ob-HS and SF-Ob-HS groups compared with the Ob-HS group. Serum isoprostane concentrations were reduced in the SBy-Ob-HS (more notably) and SF-Ob-HS groups compared with the Ob-HS and normal groups. The activities of antioxidant enzymes in tissues were enhanced, particularly in the by-product oil group. The oil extracted from by-products demonstrate anti-obesity properties (hypolipemiant, hepatoprotective, antiatherogenic, antidiabetic, and antioxidant) that may be beneficial for the management of obesity and its complications, such as hepatic steatosis.

The effect of various high-fat diet on liver histology in the development of NAFLD models in mice.

Nonalcoholic fatty liver disease (NAFLD) is exceptionally common around the world. The development of NAFLD is increasing rapidly in the world, along with changes in lifestyle. Excess lipid intake is one of the risk factors for NAFLD. The NAFLD model is induced by a high-fat diet contains SFA, MUFA, and ῳ-6 PUFA. This study aims to assess the effect of high-fat diet variation on liver histology in developing NAFLD models in mice. Thirty-six male mice (Balb/c) were divided into six groups fed a high-fat diet containing beef tallow 60%, beef tallow 45%, vegetable ghee, animal ghee+corn oil, vegetable ghee+corn oil for 28days and compared to a control group fed a chow diet. All of the mice were fed with a high-fat diet in the form of pellets ad libitum for 28days. Bodyweight and food intake were measured every day. At the last day of treatment, animals were sacrificed and the Liver were taken for histological analysis. This study showed that NAFLD model development was achieved in all group mice fed a high-fat diet with different degrees of NAFLD. Beef tallow 60% had the worst liver histology. Thus, based on this study, we found that high-fat diet variations influenced the development of NAFLD models in mice, particularly concerning liver histology.

Punicalagin Attenuates Palmitate-Induced Lipid Droplet Content by Simultaneously Improving Autophagy in Hepatocytes.

Several studies show that excessive lipid intake can cause hepatic steatosis. To investigate lipotoxicity on cellular level, palmitate (PA) is often used to highly increase lipid droplets (LDs). One way to remove LDs is autophagy, while it is controversially discussed if autophagy is also affected by PA. It is aimed to investigate whether PA-induced LD accumulation can impair autophagy and punicalagin, a natural autophagy inducer from pomegranate, can improve it. To verify the role of autophagy in LD degradation, HepG2 cells are treated with PA and analyzed for LD and perilipin 2 content in presence of autophagy inducer Torin 1 and inhibitor 3-Methyladenine. PA alone seems to initially induce autophagy-related proteins but impairs autophagic-flux in a time-dependent manner, considering 6 and 24 h PA. To examine whether punicalagin can prevent autophagy impairment, cells are cotreated for 24 h with PA and punicalagin. Results show that punicalagin preserves expression of autophagy-related proteins and autophagic flux, while simultaneously decreasing LDs and perilipin 2. Data provide new insights into the role of PA-induced excessive LD content on autophagy and suggest autophagy-inducing properties of punicalagin, indicating that punicalagin can be a health-beneficial compound for future research on lipotoxicity in liver.

Peroxiredoxin 6 Is a Key Antioxidant Enzyme in Modulating the Link between Glycemic and Lipogenic Metabolism

Insulin action and often glucose-stimulated insulin secretion are reduced in obesity. In addition, the excessive intake of lipids increases oxidative stress leading to overt type 2 diabetes mellitus (T2DM). Among the antioxidative defense systems, peroxiredoxin 6 (PRDX6) is able to reduce H2O2 and short chain and phospholipid hydroperoxides. Increasing evidences suggest that PRDX6 is involved in the pathogenesis of atherosclerosis and T2DM, but its role in the etiopathology of obesity and its complications is still not known. Therefore, in the present study, we sought to investigate this association by using PRDX6 knockout mice (PRDX6−/−). Metabolic parameters, like carbon dioxide (VCO2) production, oxygen consumption (VO2), and the respiratory exchange ratio (RER), were determined using metabolic cages. Intraperitoneal insulin and glucose tolerance tests were performed to evaluate insulin sensitivity and glucose tolerance, respectively. Liver and pancreas histochemical analyses were also evaluated. The expression of enzymes involved in lipid and glucose metabolism was analyzed by real-time PCR. Following 24 weeks of high-fat-diet (HFD), PRDX6−/− mice showed weight gain and higher food and drink intake compared to controls. VO2 consumption and VCO2 production decreased in PRDX6−/− mice, while the RER was lower than 0.7 indicating a prevalent lipid metabolism. PRDX6−/− mice fed with HFD showed a further deterioration on insulin sensitivity and glucose-stimulated insulin secretion. Furthermore, in PRDX6−/− mice, insulin did not suppress adipose tissue lipolysis with consequent hepatic lipid overload and higher serum levels of ALT, cholesterol, and triglycerides. Interestingly, in PRDX6−/− mice, liver and adipose tissue were associated with proinflammatory gene upregulation. Finally, PRDX6−/− mice showed a higher rate of nonalcoholic steatohepatitis (NASH) compared to control. Our results suggest that PRDX6 may have a functional and protective role in the development of obesity-related metabolic disorders such as liver diseases and T2DM and may be considered a potential therapeutic target against these illnesses.

2250-PUB: Fatty Acid Composition and Diabetic Kidney Disease in Type 2 Diabetes

Aim: Elevated saturated fatty acid (SFA) and decreased polyunsaturated fatty acid (PUFA) levels, especially n-3 PUFAs levels are important in the development of obesity and metabolic syndrome, but there are few accounts of the relationship between fatty acid composition and diabetic kidney disease. We investigated whether serum fatty acid composition, especially SFA and PUFA, are associated with urine albumin excretion (UAE) and estimated glomerular filtration rate (eGFR) in obese type 2 diabetic patients. Research Design and Method: The subjects were 85 patients (age: 60.3±13.9 years old, 47 male and 38 female) who were not taking EPA agents. They were divided into two groups, i.e., Obese group (n=54) with a BMI of more than 25 kg/m2 and non-Obese group (n=31) with a BMI below 25 kg/m2. Serum levels of fatty acids were measured by gas chromatography. Results: In the Obese group, the serum levels of palmitic acids and stearic acids, which belong to SFA, and dihomo-gamma-linolenic acid (DGLA), which is an n-6 PUFA, were significantly higher than those in the non-Obese group. No significant differences were seen in the serum levels of n-3 PUFA. UAE in the Obese group was 218.8±88.9 mg/gCr, which tended to be higher than that in the non-Obese group (135.9±49.0 mg/gCr), but there were no significant differences in eGFR between the two groups. The serum levels of palmitic acids, stearic acids, and DGLA showed significant positive correlations with UAE and eGFR in the Obese group, while no significant correlation was seen in the non-Obese group. Palmitic acids and DGLA were correlated with serum adiponectin and leptin levels. Conclusion: These results suggest that an excessive lipid intake may play an important role in the development of not only obesity but also diabetic kidney disease. The high levels of blood SFA and n-6 PUFA might contribute to the diabetic kidney disease progression via hyperfiltration and inflammatory effects in type 2 diabetes patients with obesity. Disclosure M. Kawai: None. R. Eto: None. F. Ayako: None. G. Sato: None. M. Hijikata: None. K. Yamashita: None. T. Ichijo: None. M. Higa: None.

Olive Oil, Palm Oil, and Hybrid Palm Oil Distinctly Modulate Liver Transcriptome and Induce NAFLD in Mice Fed a High-Fat Diet.

Nonalcoholic fatty liver disease (NAFLD) is highly prevalent worldwide. The most severe form is nonalcoholic steatohepatitis (NASH). Among risk factors for the development of NAFLD is excessive lipid intake. Since palm (P) oil is the most consumed oil in the world, we aimed to investigate the effects of high-fat diets made with P oil, hybrid palm (HP) oil, or olive (O) oil in liver. Twenty-four male mice (C57Bl/6J) were fed a high-fat diet (41% fat) containing P, HP, or O oils for 8 weeks and compared to a control (C) group fed a chow diet. Adiposity was measured with computed tomography. Body, adipose tissue, and liver weights, as well as liver fat (Bligh–Dyer), blood lipid profile, glucose, and liver enzymes were measured. Liver histology (hematoxylin–eosin) and transcriptome (microarray-based) were performed. ANOVA tests with Newman–Keuls were used. Body weight was increased in the P group (p < 0.001) and body fat in the O group (C vs. O p ≤ 0.01, P vs. O p ≤ 0.05, HP vs. O p ≤ 0.05). All high-fat diets disturbed the blood lipid profile and glucose, with marked effects of HP on very low-density lipoprotein cholesterol (VLDL), triglycerides, and alkaline phosphatase (p ≤ 0.001). HP had the highest liver fat (42.76 ± 1.58), followed by P (33.94 ± 1.13). O had a fat amount comparable to C (16.46 ± 0.34, 14.71 ± 0.70, respectively). P and HP oils induced hepatocyte ballooning. Transcriptome alterations of the O group were related to amino acid metabolism and fatty acid (FA) metabolism, the P group to calcium ion homeostasis, and HP oil to protein localization. Both P and HP oils induced NASH in mice via disturbed hepatocyte transcription. This raises concerns about the content of these oils in several industrialized foods.

Acute rumenitis due to lipid overload in a bovine

ABSTRACT: The objective of this paper is to report the epidemiological, clinical, and pathological aspects of a case of rumenitis due to the ingestion of soybean oil in a bovine. The ox had access to barrels that stored soybean oil and ingested an indeterminate amount of the product. After consuming it, the animal presented hiporexia; liquid, brownish, and greasy feces; severe dehydration (12%); apathy; sternal recumbency; and death with a clinical evolution of 4 days. At necropsy, the rumen was filled with voluminous food and moderate amount of white-gray liquid with a greasy appearance. Upon microscopic examination, hydropic degeneration of the epithelium and areas of mucosal necrosis were observed in the rumen and reticulum. From these findings, we concluded that the bovine developed a state of acidosis and acute rumenitis due to excessive intake of lipids.

Adaptations of lipid metabolism and food intake in response to low and high fat diets in juvenile grass carp (Ctenopharyngodon idellus)

This study was conducted to examine the systemic metabolic strategies of grass carp to maintain lipid homeostasis when fed with low- or high-fat diets. The isonitrogenous diets with different fat levels (9.3, 48.7 and 107.9gkg−1) were fed to grass carp for 8weeks. After the feeding trial, the growth rate and feed intake of grass carp fed with low-lipid (LL) diet or high-lipid (HL) diet were lower than fish fed with medium-lipid (ML) diet. Serum triglyceride (TG) and total body fat contents were significantly increased in grass carp with increasing lipid intake. Gene expression data indicated that fish increased hepatic gk and pk expressions to elevate glycolysis, and enhanced acc and fas expressions to accelerate biosynthesis of fatty acid (FA) to adapt to low lipid intake. Meanwhile, fish fed with LL diet decreased hepatic cpt1 expression to depress lipolysis, leading to low contents of serum TG and body fat. In contrast, excess lipid intake increased g6pase, pepck and pparα expressions to stimulate gluconeogenesis and β-oxidative, while decreased acc and fas expressions to reduce lipid synthesis in fish liver. Moreover, increased β-oxidative-induced FA or gluconeogenesis-induced serum glucose might induce the appetite suppression by high dietary fat through modulation of leptin expression. This study could be a reference in the systemic adaptation of lipid metabolism responding to dietary fat in fish. Statement of relevanceSystemic adaptation of lipid metabolism responding to dietary lipid.

Curcumin retunes cholesterol transport homeostasis and inflammation response in M1 macrophage to prevent atherosclerosis

Lipoprotein cholesterol metabolism dysfunction in the arterial wall is a major contributor to atherosclerosis, and excessive lipid intake and failed cholesterol homeostasis may accelerate the atherogenic process. Curcumin exerts multiple effects by alleviating inflammation, hyperlipidemia, and atherosclerosis; however, its role in cholesterol transport homeostasis and its underlying impact on inflammatory M1 macrophages are poorly understood. This work aimed to investigate the effect of curcumin on cholesterol transport, the inflammatory response and cell apoptosis in M1 macrophages. RAW264.7 macrophages (M0) were induced with LPS plus IFN-γ for 12 h to develop a M1 subtype and were then incubated with curcumin at different concentrations (6.25 and 12.5 μmol/L) in the presence or absence of oxLDL. Then, cholesterol influx/efflux and foam cell formation as well as inflammation and apoptosis were evaluated. It was found that curcumin increased cholesterol uptake measured by the Dil-oxLDL binding assay, and simultaneously increased cholesterol efflux carried out by Apo-A1 and HDL in M1 cells. Curcumin further reinforced ox-LDL-induced cholesterol esterification and foam cell formation as determined by Oil Red O and BODIPY staining. Moreover, curcumin dramatically reduced ox-LDL-induced cytokine production such as IL-1β, IL-6 as well as TNF-α and M1 cell apoptosis. We also found that curcumin upregulated CD36 and ABCA1 in M1 macrophages. Curcumin increased PPARγ expression, which in turn promoted CD36 and ABCA1 expression. In conclusion, curcumin may increase the ability of M1 macrophages to handle harmful lipids, thus promoting lipid processing, disposal and removal, which may support cholesterol homeostasis and exert an anti-atherosclerotic effect.

From fatty-acid sensing to chylomicron synthesis: Role of intestinal lipid-binding proteins

Today, it is well established that the development of obesity and associated diseases results, in part, from excessive lipid intake associated with a qualitative imbalance. Among the organs involved in lipid homeostasis, the small intestine is the least studied even though it determines lipid bioavailability and largely contributes to the regulation of postprandial hyperlipemia (triacylglycerols (TG) and free fatty acids (FFA)). Several Lipid-Binding Proteins (LBP) are expressed in the small intestine. Their supposed intestinal functions were initially based on what was reported in other tissues, and took no account of the physiological specificity of the small intestine. Progressively, the identification of regulating factors of intestinal LBP and the description of the phenotype of their deletion have provided new insights into cellular and molecular mechanisms involved in fat absorption. This review will discuss the physiological contribution of each LBP in the main steps of intestinal absorption of long-chain fatty acids (LCFA): uptake, trafficking and reassembly into chylomicrons (CM). Moreover, current data indicate that the small intestine is able to adapt its lipid absorption capacity to the fat content of the diet, especially through the coordinated induction of LBP. This adaptation requires the existence of a mechanism of intestinal lipid sensing. Emerging data suggest that the membrane LBP CD36 may operate as a lipid receptor that triggers an intracellular signal leading to the modulation of the expression of LBP involved in CM formation. This event could be the starting point for the optimized synthesis of large CM, which are efficiently degraded in blood. Better understanding of this intestinal lipid sensing might provide new approaches to decrease the prevalence of postprandial hypertriglyceridemia, which is associated with cardiovascular diseases, insulin resistance and obesity.

THU0289 Nutritional Status and Diet in Systemic Lupus Erythematosus

BackgroundNutritional status and intake of selected food may influence systemic lupus erythematosus (SLE) course and activity. SLE patients may have nutritional changes triggered by disease or treatment and this may...

Mécanisme d’absorption intestinale des acides gras à longue chaîne : rôle émergent du CD36

Excessive lipid intake, associated with a qualitative imbalance, favors the development of obesity and associated diseases. From organs involved in the lipid homeostasis, the small intestine remains the most poorly known although it is responsible for the lipid bioavailability and largely contributes to the regulation of postprandial hypertriglyceridemia. The mechanism of long chain fatty acid (LCFA) intestinal absorption is not totally elucidated. Over the two last decades, cloning of lipid binding proteins (LBP), proteins involved in trafficking and metabolic fate of LCFA in gut have provided new insights on cellular and molecular mechanisms involved in fat absorption. The synthesis of recent literature indicates that intestine is able to adapt its absorption capacity to the fat content of the diet. This adaptation takes place through a fat-coordinated induction of LBP and apolipoproteins. CD36 could operate as a lipid sensor responsible for a transducing signal related to the lipid content of the diet at the origin of this intestinal adaptation. This lipid-mediated metabolic response may lead to the formation of large chylomicrons rapidly degraded in the blood. All together, these new data indicate that this intestinal lipid sensing mechanism may be a therapeutic target for reducing the postprandial hypertriglyceridemia and associated cardiovascular risks.

Mitochondria and endoplasmic reticulum: Mitochondria–endoplasmic reticulum interplay in type 2 diabetes pathophysiology

Mitochondria and endoplasmic reticulum (ER) are two important metabolic organelles for the maintenance of cellular homeostasis and their functional defects are suspected to participate to the aetiology of type 2 diabetes (T2D). Particularly, excessive lipid intake and/or ectopic lipid accumulation in tissues (referred as lipotoxicity) are involved in alterations of both organelles and are closely linked to peripheral insulin resistance and defective insulin secretion. Since, mitochondria and ER are physically and functionally interconnected, their respective alterations during T2D could be interrelated. However, the mechanisms that coordinate the interplay between mitochondrial dysfunction and ER stress, and its relevance in the control of glucose homeostasis are unknown. Among these mechanisms, we will discuss on the potential role of altered mitochondria/ER crosstalk in organelle dysfunctions and in T2D pathophysiology.

The Role Played by the Peroxisome Proliferator-Activated Receptor-β/δ (PPARβ/δ) Activator, GW501516, in Control of Fatty Acid Metabolism: A New Potential Therapeutic Target for Treating Metabolic Syndrome

Obesity is increasing in significance as a global health hazard by virtue of an association with metabolic syndrome, which is characterized by abdominal obesity, hyperglycemia caused by insulin resistance, glucose intolerance, atherogenic dyslipidemia, and hypertension (1). The prevalence of obesity has increased dramatically (by about 75%) since 1980; in the United States, 33% of adults are obese and 22% have metabolic syndrome (2, 3). Although many different factors can cause metabolic syndrome, derangement of lipid homeostasis attributable to a combination of excess lipid intake and lack of physical exercise plays a major role (4). It has been suggested that adipocyte dysfunction causes excessive accumulation of intraabdominal fat that, in turn, promotes ectopic fat deposition (5–7). Recently it was shown that dyslipidemia associated with metabolic syndrome is initiated principally by hepatic overproduction of plasma lipoproteins that carry triglycerides, the very low-density lipoproteins (VLDL). Such overproduction induces a series of changes in lipoproteins, eventually resulting in the atherogenic lipid abnormalities of metabolic syndrome (8). To date, the approaches to treating the syndrome using either single drugs or drug combinations (e.g. statins, fibrates, and/or angiotensin converting enzyme inhibitors) have been less than ideal, in part because of limitations in therapeutic efficacy and drug side effects (9). Thus, it is important to develop a new and effective pharmacological therapy to prevent development of atherogenic dyslipidemia in patients with metabolic syndrome. Peroxisome proliferator-activated receptors (PPAR) are lipid-activated nuclear receptors that play multiple physiological roles, including control of fatty acid metabolism in various tissues (4). An understanding of PPAR biology could pave the way toward the development of effective therapeutic drugs for treating hypertriglyceridemia and type 2 diabetes mellitus (10). Three PPAR subtypes, namely PPAR , , and / , have been described, each of which shows distinct tissue distributions and biological activities. PPAR is mainly expressed in tissues with high fatty acid oxidation such as liver, kidney, heart, skeletal muscle, and intestine. In addition, it is expressed in vascular endothelial cells, smooth muscle cells, macrophages and T lymphocytes (11–13). Experimental and clinical studies have shown that PPAR plays a crucial role in fatty acid uptake and oxidation in the liver and heart. It is also comprised in the intake of dietary long-chain fatty acid in the gut, hepatic fatty acid synthesis, and control of inflammation (8, 11, 12). PPAR is highly expressed in white and brown adipose tissue, colon, cecum, endothelial cells, vascular smooth muscle cell, and to lesser extent in immune cells like monocytes and macrophages. PPAR is mainly involved in adipocyte proliferation and differentiation, and its agonist improves glucose homeostasis and insulin sensitivity by promoting fatty acid storage and inhibiting adipokine synthesis (8, 11, 13). PPAR / is ubiquitously expressed, but its functions were unclear until recently because no selective agonist was available. However, the development of selective

Inadequate dietary intake of children and adolescents with juvenile idiopathic arthritis and systemic lupus erythematosus

To evaluate the dietary intake of children and adolescents with juvenile idiopathic arthritis (JIA) and juvenile systemic lupus erythematosus (JSLE) using a 24-hour diet recall and relating it to the patients' clinical and anthropometric characteristics and to the drugs used in their treatment. By means of a cross-sectional study, we assessed the 24-hour diet recalls of outpatients. Their nutritional status was classified according to the CDC (2000). The computer program NutWin UNIFESP-EPM was used for food intake calculation. The Recommended Dietary Allowances and the Brazilian food pyramid were used for quantitative and qualitative analysis. Median age was 12 years for JIA patients and 16.5 years for JSLE patients. Among the JIA patients, 37.5% had active disease, and among the JSLE patients, 68.2% showed Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) > 4. Malnutrition was found in 8.3 and 4.5% of the JIA and JSLE patients, respectively, and obesity was present in 16.7 and 18.2%. For JIA patients, the excessive intake of energy, protein, and lipids was 12.5, 75, and 31.3%, respectively. For JSLE patients, the excessive intake of energy, protein, and lipids was 13.6, 86.4, and 36.4%, respectively. Low intake of iron, zinc, and vitamin A was found in 29.2 and 50, 87.5 and 86.4, and 87.5 and 95.2% of the JIA and JSLE patients, respectively. There was not a significant association between intake, disease activity, and nutritional status. Patients with rheumatic diseases have inadequate dietary intake. There is excessive intake of lipids and proteins and low intake of micronutrients.

Perception gustative des lipides alimentaires

The profound technical and economic changes of the 20th Century had a deep effect on our way of life and, consequently, on our eating behaviour. For the first time in its history, much of the world's population no longer has to “run after calories”. An abundance of food has obvious consequences: it promotes our specific appetites. Lipids account for about 40% of the calories ingested in Western countries, whereas nutritional recommendations are 5 to 10% lower. This excessive lipid intake, associated with a qualitative imbalance (excess of saturated fatty acids and cholesterol, too high ω6/ω3 ratio) strongly favours the development of obesity and associated diseases (atherosclerosis, non insulin-dependent diabetes, hypertension, cancer). This attraction to fatty foods is not specific to humans. Rats and mice spontaneously prefer lipid-rich foods if provided with a free choice. Until recently, it was thought that oral lipid detection involved only somesthesic and olfactory cues. This restrictive view has been challenged by recent observations suggesting that sense of taste is also involved in spontaneous fat preference underlying that the “fatty” taste might constitute a sixth gustatory modality. This mini-review highlights recent findings in this new field of investigations in both rodents and humans.