Increase In Triglyceride Content Research Articles

Identification of nutrition factors in the metabolic syndrome and its progression over time in older adults: analysis of the TUDA cohort

BackgroundNutrition is recognized as playing an important role in the metabolic syndrome (MetS), but the dietary components involved are unclear. We aimed to investigate nutrition factors in relation to MetS and its progression in older adults over a follow-up period of 5.4 years.MethodsCommunity-dwelling adults (≥ 60y) from the Trinity-Ulster-Department-of-Agriculture study, sampled at baseline (2008–12) and follow-up (2014–18; n 953), were classified as ‘with MetS’ by having three or more of: waist circumference (≥ 102 cm, males; ≥ 88 cm, females); HDL-cholesterol (< 1.0 mmol/L, males; < 1.3 mmol/L, females); triglycerides (≥ 1.7 mmol/L); blood pressure (systolic ≥ 130 and/or diastolic ≥ 85 mmHg); and hemoglobin A1c (≥ 39 mmol/mol).ResultsMetS was identified in 67% of participants, increasing to 74% at follow-up. Predictors at baseline for the development of metabolic syndrome (MetS) at follow-up were higher waist circumference (odds ratio [95%CI]; 1.06 [1.01–1.11]), but not BMI, and increased triglyceride concentrations (2.01 [1.29–3.16]). In dietary analysis (at follow-up), higher protein (g/kg bodyweight/day) and monounsaturated fatty acid (g/day) intakes were each associated with lower risk of MetS (0.06 [0.02–0.20] and 0.88 [0.78–1.00], respectively), whilst higher protein was also associated with lower abdominal obesity (0.10 [0.02–0.51]) and hypertension (0.22 [0.00–0.80]). Furthermore, participants with, compared to without, MetS consumed less high-quality protein foods (P = 0.006) and more low-quality protein foods (P < 0.001), as defined by the protein digestibility-corrected amino acid score.ConclusionsDietary interventions targeting protein quantity and quality may have specific benefits in preventing or delaying the progression of MetS in at-risk older people, but this requires investigation in the form of randomized trials.

Clinical effects and adverse effects of intravenous lipid emulsion treatment in dogs and cats with suspected poisoning.

This retrospective study aimed to evaluate the effects on the clinical signs of poisoning and adverse effects of intravenous lipid emulsion treatment in 82 animals (dogs and cats) with suspected poisonings over 18 months. Physical examination parameters and state of consciousness were documented every hour after the intravenous administration of a bolus of 2 ml/kg and 0.25 ml/kg/min over 60 minutes of a 20% intravenous lipid emulsion. The modified Glasgow coma scale and laboratory findings (blood gas analysis, triglyceride, lactate) were evaluated initially and three hours after discontinuing intravenous lipid emulsion administration. A statistical evaluation of the occurrence of adverse effects and the development of laboratory values was performed. A decrease in respiratory rate in the second control (8-12 hours) after ILE was observed. Three hours after completing of the intravenous lipid emulsion, triglyceride concentration increased about 10 times (p <0.001). Venous carbon dioxide partial pressure, bicarbonate, base excess, as well as the electrolytes sodium, potassium and ionized calcium decreased significantly (p <0.001). Patients who experienced a worsening of the modified Glasgow coma scale had a higher increase in triglyceride concentrations (p = 0.041) and plasma lactate (p = 0.034) and a larger decrease in bicarbonate concentrations (p = 0.053) compared to others. About 54% (n = 44) of the patients showed adverse effects which could be attributed to the administration of intravenous lipid emulsion and may be associated with a higher triglyceride increase. All of them were completely reversible within 33 hours. Adverse effects associated with intravenous lipid emulsion therapy were observed in half of the patients and were associated with a higher increase in triglycerides.

Integrated analysis of transcriptomic and physiological responses to cold stress in Macrobrachium rosenbergii

The giant freshwater prawn (GFP), Macrobrachium rosenbergii, stands out as a vital species in freshwater shrimp aquaculture. However, its susceptibility to cold conditions has increased the cost of aquaculture and limited the growth of GFP cultivation. To furnish insights at the molecular level to enhance GFP's cold tolerance, transcriptome sequencing and physiological analysis of the hepatopancreas were performed in our study. Initially, we identified 4909 differentially expressed genes (DEGs) between experimental (15 °C, 24 h) and control groups (25 °C, 24 h). These DEGs were significantly enriched in the proteasome, spliceosome, lysosome, peroxisome, and lipid metabolism-related pathways including glycerolipid metabolism, sphingolipid metabolism, linoleic acid metabolism as well as steroid hormone biosynthesis. Histological examination following various stress durations revealed a notable increase in hepatocyte vacuoles after 6 h of cold stress. Hepatocyte structure deterioration occurred in the later phase (48 h), coinciding with a significant increase in cell apoptosis. Subsequent analyses demonstrated an initial increase followed by a decrease in superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) content, while malonaldehyde (MDA) content rose with stress duration. Furthermore, a significant increase in triglyceride content and no significant change in cholesterol content was observed. RT-qPCR results unveiled significant down-regulated expression of FAS, TAGL, ACOX1, ACS and significant up-regulated expression of GPAT and DEGS. These findings suggest that oxidative stress and impaired lipid metabolism underlie the poor cold tolerance of GFP.

Targeting MYC induces lipid droplet accumulation by upregulation of HILPDA in clear cell renal cell carcinoma

Metabolic reprogramming is critical during clear cell renal cell carcinoma (ccRCC) tumorigenesis, manifested by accumulation of lipid droplets (LDs), organelles that have emerged as new hallmarks of cancer. Yet, regulation of their biogenesis is still poorly understood. Here, we demonstrate that MYC inhibition in ccRCC cells lacking the von Hippel Lindau (VHL) gene leads to increased triglyceride content potentiating LD formation in a glutamine-dependent manner. Importantly, the concurrent inhibition of MYC signaling and glutamine metabolism prevented LD accumulation and reduced tumor burden in vivo. Furthermore, we identified the hypoxia-inducible lipid droplet-associated protein (HILPDA) as the key driver for induction of MYC-driven LD accumulation and demonstrated that conversely, proliferation, LD formation, and tumor growth are impaired upon its downregulation. Finally, analysis of ccRCC tissue as well as healthy renal control samples postulated HILPDA as a specific ccRCC biomarker. Together, these results provide an attractive approach for development of alternative therapeutic interventions for the treatment of this type of renal cancer.

MiR-192-5p Ameliorates Hepatic Lipid Metabolism in Non-Alcoholic Fatty Liver Disease by Targeting Yy1.

Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. Clarifying the molecular mechanism of lipid metabolism is crucial for the treatment of NAFLD. We examined miR-192-5p levels in the livers of mice in which NAFLD was induced via a high-fat diet (HFD), as well as in mouse primary hepatocytes and human HepG2 cells treated with free fatty acids (FFAs). MiR-192-5p inhibitor was administered to NAFLD mice and hepatocytes to verify the specific function of miR-192-5p in NAFLD. We validated the target gene of miR-192-5p and further illustrated the effects of this miRNA on the regulation of triglyceride (TG) metabolism. We found that miR-192-5p was significantly increased in the livers of NAFLD mice and FFA-treated hepatocytes. Inhibition of miR-192-5p increased the accumulation of hepatic TGs and aggravated hepatic steatosis in NAFLD mice. In FFA-treated hepatocytes, miR-192-5p inhibitors markedly increased TG content, whereas overexpression of miR-192-5p reduced TG levels. Yin Yang 1 (Yy1) was identified as the target gene of miR-192-5p, which regulates TG synthesis via the YY1/fatty-acid synthase (FASN) pathway. Our results demonstrated that miR-192-5p should be considered a protective regulator in NAFLD that can inhibit hepatic TG synthesis by targeting Yy1.

Impact of early posthatch feeding on the immune system and selected hematological, biochemical, and hormonal parameters in broiler chickens

Under commercial conditions, chicks hatch within a 24 to 48 h window, a period known as the hatching window. Subsequently, they undergo various treatments before finally being transported to the broiler farm. These procedures may delay the chicks' access to food and water, sometimes receiving them as late as 72 h after hatching. Previous studies have indicated that fasting during this initial period is detrimental, leading to impaired body growth, compromised immune system response, and hindered muscle development. The objective of this study was to assess the impact of early posthatch feeding on immune system organs and selected hematological, biochemical, and hormonal parameters. The experiment utilized Ross 308 broiler eggs incubated under typical commercial hatchery conditions. The experimental group's eggs were hatched in HatchCare hatchers (HC) with immediate access to feed and water, while the control group's eggs were hatched under standard conditions (ST). Thirty chickens from each group were assessed on the 1st (D1), 7th (D7), 21st (D21), and 35th (D35) day after hatching. On D1, the HC group exhibited lower hemoglobin, hematocrit, and total serum protein values, suggesting that early access to water prevents initial dehydration in newborn chicks. Conversely, the ST group showed a stress reaction on D1 due to feed deprivation, leading to an almost 2-fold higher serum corticosterone concentration compared to the HC group. However, this increase did not result in a significant change in the heterophil/lymphocyte ratio. Furthermore, the HC group displayed an increase in triglyceride concentration and a decrease in HDL concentration on D1. On D7, the HC group exhibited an increased relative weight of the bursa and a higher CD4+ cell number in the cecal tonsil (CT), indicating a more rapid development of these organs resulting from early stimulation of the gastrointestinal tract. However, early feeding did not influence the numbers of Bu-1+, CD4+, and CD8+ cells or the germinal center (GC) areas in the spleen. In conclusion, early feeding contributes to the welfare of newborn chicks by reducing dehydration and stress levels and stimulating the development of gut-associated lymphoid tissue.

Oral sugar test responses to ertugliflozin in ten horses with insulin dysregulation

SummaryBackgroundPreliminary evidence indicates that ertugliflozin benefits horses and ponies (hereafter collectively referred to as horses) with hyperinsulinaemia and hyperinsulinaemia‐associated laminitis. The effects of ertugliflozin on the results of the oral sugar test used widely in the assessment of insulin dysregulation (ID), have not been reported.ObjectivesTo report the effects of ertugliflozin on responses to the oral sugar test (OST) in horses with ID.Study designRetrospective case series.MethodsClinical records were reviewed to identify horses with ID that had an OST (0.45 mL/kg Karo‐Light PO) performed before and after 4 days of treatment with 0.05 mg/kg ertugliflozin PO s.i.d. Pre‐ and post‐treatment insulin concentrations were compared using Wilcoxon sign‐ranked tests.ResultsTen horses with ID met the inclusion criteria. Significant reductions in plasma insulin concentration were identified at all time points after 4 days of treatment with ertugliflozin relative to pre‐treatment values. At T0 (prior to oral sugar), median insulin concentration reduced from 22.4 μu/mL (IQR: 6.5, 39) pre‐treatment to 4.8 μu/mL (IQR: 3.7, 9.2) at day 4 (p = 0.004). At T60 (60 min after oral sugar), median insulin concentration was 165 μu/mL (IQR: 61.2, 222) pre‐treatment and 78.1 μu/mL (IQR: 30.5, 137) at day 4 (p = 0.004). At T90 (90 min after oral sugar), median insulin concentration was 170 μu/mL (IQR: 88.6, 269) pre‐treatment and 84.7 μu/mL (IQR: 28.7, 122) at day 4 (p = 0.002). Serum triglyceride concentration increased from a median of 0.4 mmol/L (IQR: 0.2, 0.8) pre‐treatment to 0.9 mmol/L (IQR: 0.6, 2) at day 4 of ertugliflozin treatment (p = 0.006).Main limitationsA small heterogenous group of horses and ponies, some with PPID, were used in the absence of a control group.ConclusionsFour daily doses of ertugliflozin at 0.05 mg/kg was associated with lowering of insulin concentrations at baseline and in response to an OST in horses with ID; however, insulin levels did not return to normal in all horses. Increases in triglyceride concentrations were also observed.

221 Increasing Functional Amino Acid Ratios Does Not Improve Growth Performance in Pigs Raised Under Poor Sanitary Conditions When Fed with Individual Precision Feeding Or Conventional Feeding Systems

Abstract Immune system activation redirects dietary nutrients to defense mechanisms, thereby impairing growth performance of pigs. Supplementing pigs with functional amino acids (AA) such as Met, Thr and Trp was shown to support the immune system and reduce the negative effects on growth. However, pigs respond differently to immune stressors which increase herd variability. In this context, individual precision feeding (IPF) might be an alternative approach to reduce herd variability and increase nutrient efficiency in immune challenged pigs. This study aimed to evaluate growth performance, body composition, nitrogen (N) efficiency and haptoglobin and triglycerides serum concentration in growing pigs raised in poor sanitary conditions (PoorSC). The PoorSC was characterized by oral inoculation with 2 × 109 cfu of Salmonella typhimurium and manure spreading on the pen floor. Sixty gilts (23 ± 2.8 kg BW) were distributed in BW blocks according to a 2 dietary (D) × 2 feeding system (FS) factorial arrangement composed of to 2 diets [control (CN): INRA ideal AA ratio or supplemented (AA+) 120% of the ideal ratio for Met, Thr and Trp] and 2 feeding systems [conventional (GP) or IPF]. GP pigs were fed with a unique diet that matched the SID Lys requirement of the 80th-percentile pig at the beginning of the trial whereas the IPF pigs received a diet tailored daily to each pig requirement. All pigs were housed in the same pen and fed ad libitum during 28 experimental days with automatic feeding stations able to provide to each pig the assigned diet. Body composition was obtained by dual X-ray absorptiometry at days 0 and 28 and blood samples were collected at d 28. Data were analyzed with D and FS and their interaction as main fixed factors and body weight (BW) blocks as a random effect (Table 1). Haptoglobin serum concentration increased from d 0 to 28 regardless of FS and D (P &amp;lt; 0.10). IPF pigs fed with CN diet had the lightest BW at the end of the trial (P ≤ 0.10; FS × D), whereas BW was similar for the other treatments. However, across diets, IPF pigs had final BW, and protein, ADG, G:F, protein and lipid deposition, N intake and excretion and circulating triglycerides that were less than GP pigs. N utilization efficiency was similar across treatments. Additionally, increasing the provision of the studied functional AA did not improve pig performance. Thus, showing no benefits in increasing AA ratios for growth and immune response. The increased triglycerides concentration and low protein and lipid deposition suggests that IPF pigs prioritized the immune system to the expense of protein and lipid accretion. In conclusion, AA supplementation and IPF do not improve growth performance and N efficiency of pigs raised in poor sanitary conditions.

The metabolic response of human trophoblasts derived from term placentas to metformin

Aims/hypothesisMetformin is increasingly used therapeutically during pregnancy worldwide, particularly in the treatment of gestational diabetes, which affects a substantial proportion of pregnant women globally. However, the impact on placental metabolism remains unclear. In view of the association between metformin use in pregnancy and decreased birthweight, it is essential to understand how metformin modulates the bioenergetic and anabolic functions of the placenta.MethodsA cohort of 55 placentas delivered by elective Caesarean section at term was collected from consenting participants. Trophoblasts were isolated from the placental samples and treated in vitro with clinically relevant doses of metformin (0.01 mmol/l or 0.1 mmol/l) or vehicle. Respiratory function was assayed using high-resolution respirometry to measure oxygen concentration and calculated {dot{V}mathrm{O}}_{2}. Glycolytic rate and glycolytic stress assays were performed using Agilent Seahorse XF assays. Fatty acid uptake and oxidation measurements were conducted using radioisotope-labelled assays. Lipidomic analysis was conducted using LC-MS. Gene expression and protein analysis were performed using RT-PCR and western blotting, respectively.ResultsComplex I-supported oxidative phosphorylation was lower in metformin-treated trophoblasts (0.01 mmol/l metformin, 61.7% of control, p<0.05; 0.1 mmol/l metformin, 43.1% of control, p<0.001). The proton efflux rate arising from glycolysis under physiological conditions was increased following metformin treatment, up to 23±5% above control conditions following treatment with 0.1 mmol/l metformin (p<0.01). There was a significant increase in triglyceride concentrations in trophoblasts treated with 0.1 mmol/l metformin (p<0.05), particularly those of esters of long-chain polyunsaturated fatty acids. Fatty acid oxidation was reduced by ~50% in trophoblasts treated with 0.1 mmol/l metformin compared with controls (p<0.001), with no difference in uptake between treatment groups.Conclusions/interpretationIn primary trophoblasts derived from term placentas metformin treatment caused a reduction in oxidative phosphorylation through partial inactivation of complex I and potentially by other mechanisms. Metformin-treated trophoblasts accumulate lipids, particularly long- and very-long-chain polyunsaturated fatty acids. Our findings raise clinically important questions about the balance of risk of metformin use during pregnancy, particularly in situations where the benefits are not clear-cut and alternative therapies are available.Graphical

Sensing of triglyceride concentration in blood solution using photoacoustic microscopy.

The level of triglyceride (TG) in blood is essential to human health, and hypertriglyceridemia (TG level > 150 mg/dL) would lead to cardiovascular disease and acute pancreatitis that threaten human life. Routine methods for measuring the TG level in blood depend on a lipid panel blood test, which is invasive and not convenient. Here, we use photoacoustic (PA) microscopy to test the PA amplitude of blood solutions (based on hemoglobin powder as well as flowing sheep blood) with different TG concentrations. Interestingly, we observe that the PA amplitude increases with increasing TG concentration in blood solutions, which is attributed to the increase of the Grüneisen coefficient. The preliminary in vitro study shows that the PA methodology is able to detect the TG level down to 450 mg/dL. This finding provides an opportunity for using photoacoustics to noninvasively diagnose hypertriglyceridemia.

Neonatal administration of fenofibrate had no developmental programming effect on the lipid profile and relative leucocyte telomere lengths of adolescent rats fed a high-fructose diet postnatally.

Telomere length, a marker of ageing, is susceptible to developmental programming that may cause its accelerated attrition. Metabolic syndrome triggers telomere attrition. Fenofibrate, a peroxisome proliferator-activated receptor-alpha agonist, is protective against telomere attrition. We investigated the impact of fenofibrate administered during suckling on the lipid profile and leucocyte telomere lengths of rats fed a high-fructose diet post-weaning. Suckling Sprague-Dawley pups (n=119) were allocated to four groups and gavaged with either 10mL·kg-1 body mass 0.5% dimethyl sulfoxide, 100mg·kg-1 body mass fenofibrate, fructose (20%, w / v), or a combination of fenofibrate and fructose for 15 days. Upon weaning, each of the initial groups was split into two subgroups: one had plain water while the other had fructose solution (20%, w / v) to drink for 6 weeks. Blood was collected for DNA extraction and relative leucocyte telomere length determination by real-time PCR. Plasma triglycerides and cholesterol were also quantified. The treatments had no effect (p>0.05) on body mass, cholesterol concentration, and relative leucocyte telomere lengths in both sexes. Post-weaning fructose increased triglyceride concentrations (p<0.05) in female rats. Fenofibrate administered during suckling did not affect ageing nor did it prevent high fructose-induced hypertriglyceridaemia in female rats.

Exposure to 6-PPD quinone enhances lipid accumulation through activating metabolic sensors of SBP-1 and MDT-15 in Caenorhabditis elegans

Although it has been shown that exposure to 6-PPDQ can cause toxicity on environmental organisms, its possible effects on metabolic state remain largely unclear. We here determined the effect of 6-PPDQ exposure on lipid accumulation in Caenorhabditis elegans. We observed increase in triglyceride content, enhancement in lipid accumulation, and increase in size of lipid droplets in 6-PPDQ (1–10 μg/L) exposed nematodes. This detected lipid accumulation was associated with both increase in fatty acid synthesis reflected by increased expressions of fasn-1 and pod-2 and inhibition in mitochondrial and peroxisomal fatty acid β-oxidation indicated by decreased expressions of acs-2, ech-2, acs-1, and ech-3. The observed lipid accumulation in 6-PPDQ (1–10 μg/L) exposed nematodes was also related to the increase in synthesis of monounsaturated fatty acylCoAs reflected by altered expressions of fat-5, fat-6, and fat-7. Exposure to 6-PPDQ (1–10 μg/L) further increased expressions of sbp-1 and mdt-15 encoding two metabolic sensors to initiate the lipid accumulation and to regulate the lipid metabolism. Moreover, the observed increase in triglyceride content, enhancement in lipid accumulation, and alterations in fasn-1, pod-2, acs-2, and fat-5 expressions in 6-PPDQ exposed nematodes were obviously inhibited by sbp-1 and mdt-15 RNAi. Our observations demonstrated the risk of 6-PPDQ at environmentally relevant concentration in affecting lipid metabolic state in organisms.

Hypertension and psychosis.

Hypertension, a prevalent component of metabolic syndrome (MetS), is a well-known risk factor for cardiovascular diseases (CVD). Psychosis is a feature in the schizophrenia spectrum. Meta-analysis suggests that the prevalence of hypertension in schizophrenia and related disorders is 39%. This may be explained by a unidirectional association between hypertension and psychosis, in that psychosis can be a causative factor of hypertension via antipsychotic medication, inflammation and irregular autonomic nervous system activity through multiple mechanisms. Obesity is a side effect of antipsychotic medication and is a risk factor for hypertension. Obesity leads to raised blood pressure, atherosclerosis, increased triglyceride concentration and decreased high-density lipoprotein concentration. Inflammation accompanies hypertension and obesity. In recent years, the role of inflammation in the onset of psychosis has been increasingly recognised. It underlies the immune dysregulation observed in both schizophrenia and bipolar disorder. Interleukin-6, a marker and driver of inflammation, is related to obesity and plays a role in the pathogenesis of MetS and hypertension. The lack of preventive care of hypertension and other MetS risk factors for patients on antipsychotic medication is reflected in the high incidence of CVD in this population. It is important to detect and treat MetS and hypertension in patients with psychosis in order to reduce cardiovascular morbidity and mortality in this population.

Asymmetric dimethylarginine positively modulates calcium-sensing receptor signalling to promote lipid accumulation

Asymmetric dimethylarginine (ADMA) is generated through the irreversible methylation of arginine residues. It is an independent risk factor for cardiovascular disease, currently thought to be due to its ability to act as a competitive inhibitor of the nitric oxide (NO) synthase enzymes. Plasma ADMA concentrations increase with obesity and fall following weight loss; however, it is unknown whether they play an active role in adipose pathology. Here, we demonstrate that ADMA drives lipid accumulation through a newly identified NO-independent pathway via the amino-acid sensitive calcium-sensing receptor (CaSR). ADMA treatment of 3T3-L1 and HepG2 cells upregulates a suite of lipogenic genes with an associated increase in triglyceride content. Pharmacological activation of CaSR mimics ADMA while negative modulation of CaSR inhibits ADMA driven lipid accumulation. Further investigation using CaSR overexpressing HEK293 cells demonstrated that ADMA potentiates CaSR signalling via Gq intracellular Ca2+ mobilisation. This study identifies a signalling mechanism for ADMA as an endogenous ligand of the G protein-coupled receptor CaSR that potentially contributes to the impact of ADMA in cardiometabolic disease.

Integrated miRNA-mRNA analysis reveals the dysregulation of lipid metabolism in mouse liver induced by developmental arsenic exposure.

Developmental arsenic exposure leads to increased susceptibility to liver diseases including nonalcoholic fatty liver diseases, but the mechanism is incompletely understood. In this study, C57BL/6J mice were used to establish a lifetime arsenic exposure model covering developmental stage. We found that arsenic-exposed offspring in later life showed hepatic lipid deposition and increased triglyceride content. Despite no significant hepatic pathological changes in the offspring at weaning, 86 miRNAs and 136 mRNAs were differentially expressed according to miRNA array and mRNA sequencing. The differentially expressed genes (DEGs) were crossed with the target genes predicted by differentially expressed miRNAs (DEMs), and 47 differentially expressed target genes (DETGs) were obtained. Functional annotation suggested that lipid metabolism related pathways were significantly enriched. The pivotal regulator in the four major pathways to maintain liver lipid homeostasis were further determined, with significant alterations found in FABP5, SREBP1, ACOX1 and EHHADH. Of note, miRNA-mRNA integration analysis revealed that miR-7118-5p, miR-7050-5p, miR-27a/b-3p, and miR-103-3p acted as key regulators of fatty acid metabolism genes. Taken together, miRNA-mRNA integration analysis indicates that the lipid metabolism pathway in the liver of weaned mice was dysregulated by developmental arsenic exposure, which may contribute to the development of NAFLD in later life.

Postprandial Lipid Response Following a High Fat Meal in Rats Adapted to Dietary Fiber

Rats were adapted to diets containing 5 g/100 g cellulose (CL), 5 g/100 g oat bran fiber (OB) or 5 g/100 g psyllium husk (Psy) for 4 wk. Following a 12-h fast, animals were either killed at 0 h (baseline) or fed 4.5 g of a test meal that provided 50% energy from fat, then killed at 1, 4 or 6 h postprandially. Fasting plasma and HDL cholesterol concentrations were lower in Psy-fed animals than in rats fed either CL or OB. Plasma triglycerides increased significantly from baseline (0 h) in all groups but did not differ among diet treatments. Increases in triglyceride content of the chylomicron/VLDL fraction occurred in the CL- and OB-fed groups and in the HDL fraction of the Psy-fed group during the postprandial period. In unfed animals the hepatic and intestinal levels of apolipoprotein A-IV mRNA were higher in the CL-fed group than in the groups fed OB and Psy. Apolipoprotein B mRNA was higher in the intestine of the OB-fed group than in the groups fed CL and Psy and had a significant gradient along the small intestine, increasing in the distal third. The results suggest that chronic consumption of fiber is less likely to modify the acute plasma triglyceride response to a fat-containing test meal than if a fiber supplement is incorporated into the meal.

Impaired white adipose tissue fatty acid metabolism in mice fed a high-fat diet worsened by arsenic exposure, primarily affecting retroperitoneal adipose tissue

Fatty acid (FA) metabolism dysfunction of white adipose tissue (WAT) underlies obesity and insulin resistance in response to high calorie intake and/or endocrine-disrupting chemicals (EDCs), among other factors. Arsenic is an EDC that has been associated with metabolic syndrome and diabetes. However, the combined effect of a high-fat diet (HFD) and arsenic exposure on WAT FA metabolism has been little studied.FA metabolism was evaluated in visceral (epididymal and retroperitoneal) and subcutaneous WAT of C57BL/6 male mice fed control or HFD (12 and 40% kcal fat, respectively) for 16 weeks together with an environmentally relevant chronic arsenic exposure through drinking water (100 μg/L) during the second half of the study.In mice fed HFD, arsenic potentiated the increase of serum markers of selective insulin resistance in WAT and fatty acid re-esterification and the decrease of the lipolysis index. Retroperitoneal was the WAT most affected, where the combination of arsenic and HFD in contrast to HFD, generated higher adipose weight, larger adipocytes, increased triglyceride content, and decreased fasting stimulated lipolysis evidenced by lower phosphorylation of HSL and perilipin. At the transcriptional level, arsenic in mice fed either diet downregulated genes involved in fatty acid uptake (LPL, CD36), oxidation (PPARα, CPT1), lipolysis (ADRß3) and glycerol transport (AQP7 and AQP9). Additionally, arsenic potentiated hyperinsulinemia induced by HFD, despite a slight increase in weight gain and food efficiency.Thus, the second hit of arsenic in sensitized mice by HFD worsens fatty acid metabolism impairment in WAT, mainly retroperitoneal, along with an exacerbated insulin resistance phenotype.

Effect of Clinical and Laboratory Parameters on HDL Particle Composition.

The functional status of High-Density Lipoprotein (HDLs) is not dependent on the cholesterol content but is closely related to structural and compositional characteristics. We reported the analysis of HDL lipidome in the healthy population and the influence of serum lipids, age, gender and menopausal status on its composition. Our sample comprised 90 healthy subjects aged between 30 and 77 years. HDL lipidome was investigated by Nuclear Magnetic Resonance (NMR) spectroscopy. Among serum lipids, triglycerides, apoAI, apoB and the ratio HDL-C/apoAI had a significant influence on HDL lipid composition. Aging was associated with significant aberrations, including an increase in triglyceride content, lysophosphatidylcholine, free cholesterol, and a decrease in esterified cholesterol, phospholipids, and sphingomyelin that may contribute to increased cardiovascular risk. Aging was also associated with an atherogenic fatty acid pattern. Changes occurring in the HDL lipidome between the two genders were more pronounced in the decade from 30 to 39 years of age and over 60 years. The postmenopausal group displayed significant pro-atherogenic changes in HDLs compared to the premenopausal group. The influence of serum lipids and intrinsic factors on HDL lipidome could improve our understanding of the remodeling capacity of HDLs directly related to its functionality and antiatherogenic properties, and also in appropriate clinical research study protocol design. These data demonstrate that NMR analysis can easily follow the subtle alterations of lipoprotein composition due to serum lipid parameters.

The fat burning ability of melatonin during submaximal exercise

ABSTRACT The regulation of the balance between glucose and lipid use during exercise has gained increasing attention in the last decades. The contribution of fat and glucose to energy expenditure can be modulated by hormones and other endogenous factors. The increase in melatonin during exercise may be linked to an enhancement in lipid utilization, reflected by an increase in triglyceride concentration. The purpose of this study was to explore the effect of daytime melatonin administration on plasma glucose, triglycerides, and cortisol responses to submaximal exercise. Eight physical education students were asked to run for 45 minutes at 60% of their maximum aerobic speed after 50 minutes of either melatonin-(6 mg) or placebo consumption. Cortisol, triglycerides, and glucose were measured in plasma samples before and immediately after exercise. Post-exercise cortisol, triglycerides, and glucose levels were corrected for fluid shifts. In both conditions , post-exercise cortisol significantly increased (by ≥20%) . Post-exercise glucose levels significantly increased only in the placebo condition . However, post-exercise triglyceride levels significantly increased only in the melatonin condition. To conclude, acute melatonin administration decreases the glucose response while increasing triglycerides’ response to exercise. Therefore, it would be possible to suggest that exogenous melatonin administration before endurance exercise could promote fat burning.

Features of metabolic disorders in centenarians

Aim: to study the features of purine, lipid and carbohydrate metabolic disorders in patients with coronary artery disease over 90 years old (centenarians).Materials and methods. The study enrolled 225 patients over 90 years, hospitalized with coronary artery disease. The majority of patients (67.6%) were women. The mean age of the patients reached 92.5+2.2 years (from 90 to 106 years).The blood levels of uric acid, lipids, glucose and body mass index were determined.Results. Obesity was registered in 31.5% of patients, grade III obesity – in 1 patient. Overweight was observed in 39.1% of patients, normal body mass index (BMI) – in 28.9%. An increase in the blood concentration of triglycerides was determined in 11.2% of patients. A decrease in the level of high-density lipoprotein (HDL) cholesterol was registered in 12.7% of patients. The blood concentration of low-density lipoprotein cholesterol (LDL) less than 2.0 mmol/l was observed in 23.3% of cases. Dyslipidemia was registered more often in women (p=0.02). Hyperuricemia was found in 37.3% of patients – in 41.4% of women and 28.8% of men (p=0.04). Elevated fasting blood glucose levels were determined in 23.1% of patients, but only 0.9% of patients had glucose levels above 14 mmol/l.Conclusion. The study results indicate some features of metabolic disorders in centenarians with coronary artery disease. Most of the patients were obese or overweight. Frequent hyperuricemia was registered, but relatively low levels of atherogenic lipids and glucose.