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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 91 records · Page 5
All sourcesNASA NTRSDOE OSTI
DOE OSTI2019

Juxtatumoral perinephric fat analysis in clear cell renal cell carcinoma

Purpose: The purpose of the study was to evaluate the feasibility of using contrast-enhanced computed tomography (CECT)-based texture analysis (CTTA) metrics to differentiate between juxtatumoral perinephric fat (JPF) surrounding low-grade (ISUP 1–2) versus high-grade (ISUP 3–4) clear cell renal cell carcinoma (ccRCC). Methods: In this IRB-approved study, we retrospectively queried the surgical database between June 2009 and April 2016 and identified 83 patients with pathologically confirmed ccRCC (low grade: n = 54, mean age = 61.5 years, 18F/35M; high grade n = 30, mean age = 61.7 years, 8F/22M) who also had pre-operative multiphase CT acquisitions. CT images were transferred to a 3D workstation, and nephrographic phase JPF regions were manually segmented. Using an in-house developed Matlab program, a CTTA panel comprising of texture metrics extracted using six different methods, histogram, 2D- and 3D-Gray-level co-occurrence matrix (GLCM) and Gray-level difference matrix (GLDM), and 2D-Fast Fourier Transform (FFT) analyses, was applied to the segmented images to assess JPF textural heterogeneity in low- versus high-grade ccRCC. Univariate analysis and receiver-operator characteristics (ROC) analysis were used to assess interclass differences in texture metrics and their prediction accuracy, respectively. Results: All methods except GLCM consistently revealed increased heterogeneity in the JPF surrounding high- versus low-grade ccRCC. FFT showed increased complexity index (p < 0.01). Histogram analysis showed increased kurtosis and positive skewness in (p < 0.03), and GLDM analysis showed decreased measure of correlation coefficient (MCC) (p < 0.04). Several of the GLCM metrics showed statistically significant (p < 0.04) textural differences between the two groups, but with no consistent trend. ROC analysis showed that MCC in GLCM analysis had an area under the curve of 0.75. Conclusions: Our study suggests that CTTA of ccRCC shows statistically significant textural differences in JPF surrounding high- versus low-grade ccRCC.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2019

Withaferin A Protects Against High-Fat Diet–Induced Obesity Via Attenuation of Oxidative Stress, Inflammation, and Insulin Resistance

Withaferin A (WA), a bioactive constituent derived from Withania somnifera plant, has been shown to exhibit many qualifying properties in attenuating several metabolic diseases. The current investigation sought to elucidate the protective mechanisms of WA (1.25 mg/kg/day) on pre-existing obese mice mediated by high-fat diet (HFD) for 12 weeks. Following dietary administration of WA, significant metabolic improvements in hepatic insulin sensitivity, adipocytokines with enhanced glucose tolerance were observed. The hepatic oxidative functions of obese mice treated with WA were improved via augmented antioxidant enzyme activities. The levels of serum pro-inflammatory cytokines and hepatic mRNA expressions of toll-like receptor (TLR4), nuclear factor κB (NF-κB), tumor necrosis factor-α (TNF-α), chemokine (C-C motif) ligand-receptor, and cyclooxygenase 2 (COX2) in HFD-induced obese mice were reduced. Mechanistically, WA increased hepatic mRNA expression of peroxisome proliferator-activated receptors (PPARs), cluster of differentiation 36 (CD36), fatty acid synthase (FAS), carnitine palmitoyltransferase 1 (CPT1), glucokinase (GCK), phosphofructokinase (PFK), and phosphoenolpyruvate carboxykinase (PCK1) that were associated with enhanced lipid and glucose metabolism. Taken together, these results indicate that WA exhibits protective effects against HFD-induced obesity through attenuation of hepatic inflammation, oxidative stress, and insulin resistance in mice.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Metabolic biomarkers for non-alcoholic fatty liver disease induced by high-fat diet: In vivo magnetic resonance spectroscopy of hyperpolarized [1-{sup 13}C] pyruvate

Hyperpolarized {sup 13}C magnetic resonance spectroscopy (MRS) to assess hepatic metabolism in non-alcoholic fatty liver disease (NAFLD) has not been reported. This study searched for cellular metabolism-based biomarkers for NAFLD induced by a high-fat diet (HFD) in rats. Also, correlations of the biomarkers with enzyme levels and histopathology were identified during a 6-week follow-up. Six rats were fed a control diet (CD) and seven rats were fed the HFD for 6 weeks. Hyperpolarized {sup 13}C dynamic MRS was performed on rat liver following an injection of hyperpolarized [1-{sup 13}C] pyruvate. Compared with CD-fed rats, HFD-fed rats showed significant increases in the levels of serum alanine aminotransferase and low-density lipoprotein cholesterol at weeks 4 and 6 of follow-up. After the 6-week HFD, the ratios of [1-{sup 13}C] alanine/pyruvate and [1-{sup 13}C] lactate/pyruvate were significantly increased, as were the levels of alanine aminotransferase and lactate dehydrogenase, which are potentially associated with hepatosteatosis. The results implicate [1-{sup 13}C] alanine and [1-{sup 13}C] lactate as potentially useful noninvasive biomarkers of hepatosteatosis occurring in NAFLD. - Highlights: • Hyperpolarized {sup 13}C-alanine and lactate are noninvasive biomarkers on hepatosteatosis. • During the course of HFD feeding, {sup 13}C-alanine and lactate were increased in HFD-rats. • Hyperpolarized {sup 13}C dynamic MRS will be helpful to monitor the progression of NAFLD.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Beneficial effects of paeoniflorin on osteoporosis induced by high-carbohydrate, high-fat diet-associated hyperlipidemia in vivo

Highlights: • Paeoniflorin significantly improved the serum lipid profile. • Paeoniflorin restored trabecular and cortical parameters, and the biomechanical strength. • Paeoniflorin reversed the hyperlipidemia associated-symptoms in the rat model. Osteoporosis is linked to reduced bone mineral density (BMD) as a major risk factor for fragility fractures. Recent studies indicated an association between BMD and abnormally elevated lipid levels in blood as common indicators for hyperlipidemia. In this study, we assessed the protective effect of paeoniflorin, a phytochemical compound with multiple pharmacological activities, against hyperlipidemia-induced osteoporosis in rats fed a high-carbohydrate, high-fat diet (HCHF). The special diet-fed rats were subjected to an 8-week treatment with either paeoniflorin (20 mg/kg, daily) or vehicle. The control group received a normal diet during the entire study. At study conclusion, serum markers of lipid metabolism and bone turnover were measured. Bone strength was assessed by biomechanical testing, and femurs were scanned using micro-computed tomography to analyze trabecular and cortical bone structure. Interestingly, paeoniflorin controlled the serum lipid profile by significantly decreasing HCHF-induced high levels of total cholesterol, triglyceride, and low-density lipoprotein cholesterol. Paeoniflorin significantly improved trabecular and cortical parameters as well as femur length and width that were negatively affected by HCHF diet. Biomechanical strength testing showed that femurs of HCHF diet-fed rats endured significantly lower force but higher displacement and strain than those of control rats, whereas paeoniflorin reversed the negative effects. Moreover, paeoniflorin rescued osteoblast differentiation and cell spreading activities along with bone turnover markers. In conclusion, HCHF-induced hyperlipidemia caused adverse effects on the bone that were rescued by paeoniflorin treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

NFATc3 deficiency protects against high fat diet (HFD)-induced hypothalamus inflammation and apoptosis via p38 and JNK suppression

Highlights: • NFATc3 expression is increased in HFD-induced hypothalamus. • NFATc3-knockout attenuates HFD-induced metabolic syndrome in mice. • NFATc3-deletion alleviates inflammation and apoptosis in hypothalamus of HFD-fed mice. • NFATc3-ablation reduces inflammation and apoptosis in fructose-stimulated astrocytes via p38 and JNK activation. Hypothalamic inflammation and apoptosis cause neural injury, playing an important role in metabolic syndrome development. Nuclear Factors of Activated T cells (NFATc3) show many physiological and pathological effects. However, the function of NFATc3 in high fat diet (HFD)-induced hypothalamus injury remains unknown. The wild type (WT) and NFATc3-knockout (KO) mice were subjected to HFD feeding for 16 weeks to examine NFATc3 function in vivo. Astrocytes isolated from WT or KO mice were cultured and exposed to fructose (Fru) in vitro. The liver damage, hypothalamus injury, pro-inflammatory markers, NF-κB (p65), Caspase-3 and mitogen-activated protein kinases (MAPKs) pathways were evaluated. NFATc3 was significantly up-regulated in hypothalamus from mice challenged with HFD, and in astrocytes incubated with Fru. Both in vivo and in vitro studies indicated that NFATc3-deletion attenuated metabolism syndrome, reduced inflammatory regulators expression, inactivated NF-κB (p65), Caspase-3 and p38/JNK signaling pathway. Of note, we identified that promoting p38 or JNK activation could rescue inflammatory response and apoptosis in NFATc3-KO astrocytes stimulated by Fru. Together, these findings revealed an important role of NFATc3 NFATc3 for HFD-induced metabolic syndrome and particularly hypothalamus injury, and understanding of the regulatory molecular mechanism might provide new and effective therapeutic strategies for prevention and treatment of hypothalamic damage associated with dietary obesity-associated neuroinflammation and apoptosis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Sennoside A protects mitochondrial structure and function to improve high-fat diet-induced hepatic steatosis by targeting VDAC1

Highlights: • SA inhibited VDAC1 expression in livers of HFD-induced hepatic steatosis mice. • SA suppressed the ATP surplus by inhibiting mitochondrial complex I in livers of HFD-induced hepatic steatosis mice. • SA protected mitochondrial function and structure in livers of HFD-induced hepatic steatosis mice. • SA improved HFD-induced hepatic steatosis and hepatomegaly. Mitochondrial dysfunction is mainly associated with high-fat-diet (HFD)-induced hepatic steatosis. Sennoside A (SA), a commonly used clinical stimulant laxative, is reported to improve energy metabolism and insulin resistance. However, the effect and mechanism of SA on HFD-induced hepatic steatosis remain largely unknown. The aim of this study was to determine the effect and mechanism of SA on HFD-induced hepatic steatosis in mice. We examined the liver and body weight of mice to evaluate the physical changes in the liver. Hematoxylin and eosin (H&E) and oil red O staining were used to detect the lipid accumulation. The mitochondrial structure and function were tested by transmission electron microscopy and the Seahorse XF24 Analyzer. Furthermore, mitochondrial complexes I, II, and IV and voltage-dependent anion channel 1 (VDAC1) protein activity were detected to understand the mechanism of the protective effect on mitochondria. As a result, damage to the structure and function in the hepatic mitochondria of HFD-induced hepatic steatosis was observed in mice. The structural damage was in the form of loss of cristae, mitochondrial swelling, vacuolization and even rupturing of the outer mitochondrial membrane (OMM). Functional alterations were found by activation of complex I and deficiency in complexes II and IV. The VDAC1 activity and the total ATP in the liver tissue was increased under hepatic steatosis conditions. The above effects were reversed by SA. These data suggest that inhibition of VDAC1 may be an underlying mechanism of SA for protecting mitochondria in HFD-induced hepatic steatosis in mice. Thus, VDAC1 may be a promising target for treating fatty liver disease.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Suppression of NF-κB activation by PDLIM2 restrains hepatic lipogenesis and inflammation in high fat diet induced mice

Highlights: • PDLIM2 deficiency promotes HFD-induced mice obesity and insulin resistance. • PDLIM2 deficiency promotes hepatic dyslipidemia in HFD-induced mice. • PDLIM2 deficiency intensifies HFD-induced hepatic inflammation. • Reducing NF-κB activation attenuates PDLIM2 deficiency-exacerbated inflammation and dyslipidemia in PAL-treated primary hepatocytes. Non-alcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis, insulin resistance, dyslipidemia and a systemic pro-inflammatory response, a leading cause of cirrhosis and hepatocellular carcinoma. Here, we showed that PDZ-LIM domain-containing protein 2 (PDLIM2) was an effective suppressor of steatohepatitis. After 16 weeks on a high fat diet (HFD), obesity, insulin resistance, hepatic dyslipidemia and inflammation were markedly aggravated in PDLIM2-knockout (KO) mice. PDLIM2 deletion resulted in lipid accumulation in liver tissue samples of HFD-induced mice, as evidenced by the significant increase of hepatic TG and TC through reducing the expression of lipogenesis- and transcriptional regulators of lipid metabolism-related genes and enhancing fatty acid oxidation-associated molecules. In addition, PDLIM2-ablation promoted the expression of pro-inflammatory cytokines by activating nuclear factor kappa-B (NF-κB) signaling pathway, as supported by the remarkable increase of phosphorylated IKKβ, IκBα and NF-κB expressions in liver of HFD-fed mice. Of note, the in vitro study demonstrated that PDLIM2 ablation-enhanced inflammatory response and disorder of lipid metabolism were abrogated by suppressing NF-κB activity. Collectively, the findings could lead to the development of potential therapeutic strategy to prevent NAFLD and associated metabolic disorders by targeting PDLIM2.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

TLR4 mediates high-fat diet induced physiological changes in mice via attenuating PPARγ/ABCG1 signaling pathway

High-fat diet (HFD) is known to promote atherosclerosis which accelerates the development of atherosclerotic cardiovascular diseases. Vascular dysfunction characterized by inflammation and lipid accumulation is common in atherosclerosis caused by HFD. The specific effects of HFD on blood vessels and the underlying mechanisms need to be further clarified. Toll-like receptor 4 (TLR4) is a key contributing factor in atherosclerosis and TLR4 deficiency protects vascular smooth muscle cells against inflammatory responses and lipid accumulation in vitro. However, the physiological significance of TLR4 signaling in HFD-induced changes is unknown. In this study, we observed that HFD feeding increased body weight, circulating inflammatory cytokines and lipid accumulation in the aorta of wild-type mice but apart from increasing body weight, did not affect the TLR4 knockout mice. TLR4 expression increased significantly in the arterial walls after receiving HFD treatment, while that of the co-localizing PPARγ and ABCG1 markedly decreased. TLR4 deficiency reversed the HFD-induced attenuation of PPARγ and ABCG1. In conclusion, TLR4 mediates HFD induced increase in body weight, inflammation and aortic lipid accumulation through, at least partly, the PPARγ/ABCG1 signaling pathway. Therefore, interfering with TLR4 signaling is a viable therapeutic option in diet induced atherosclerosis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Up regulated Tmbim1 activation promotes high fat diet (HFD)-induced cardiomyopathy by enhancement of inflammation and oxidative stress

Highlights: • Tmbim1 deletion exacerbates metabolic syndrome in HFD-fed mice. • Tmbim1 knockout aggravates HFD-induced cardiac inflammation and oxidative stress. • Tmbim1-regulated cardiac injury is tightly associated with inflammation and oxidative stress in PA-treated primary cardiomyocytes. The prevalence of cardiomyopathy due to metabolic stress has up-regulated dramatically; nevertheless, its molecular mechanisms remain unclear. Here we suggested that transmembrane BAX inhibitor motif-containing 1 (Tmbim1) is down-regulated in the hearts of mice fed with high fat diet (HFD). We provided evidence that Tmbim1 knockout (KO) accelerated HFD-induced metabolic disorders in mice, as supported by the remarkable increase of fasting serum glucose and insulin levels. HFD-induced cardiac dysfunctions were greatly intensified by the loss of Tmbim1, along with higher levels of lactate dehydrogenase (LDH) and creatine kinase (CK) in serum. In addition, Tmbim1 deletion significantly enhanced lipid accumulation in heart of mice administrated with HFD. Furthermore, Tmbim1 knockout reinforced myocardial inflammation, evidenced by increasing the expression of pro-inflammatory cytokines (interleukin 1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α)), and the activation of nuclear factor-κB (NF-κB) signaling pathway. Tmbim1 deficiency strengthened oxidative damage in hearts of HFD-fed mice, accompanied with a significant reduction of nuclear factor-erythroid 2 related factor 2 (Nrf-2) pathway. In palmitate (PA)-treated primary cardiomyocytes, Tmbim1 ablation markedly enhanced cell inflammation and oxidative stress, which were abolished by the suppression of ROS generation and NF-κB activation. Taken together, these findings suggested that Tmbim1 might be a key suppressor of metabolic stress-induced cardiomyopathy, which could be a promising target for the treatment of metabolic syndrome-triggered myocardial damage and heart failure.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Intestinal epithelial cell-specific Raptor is essential for high fat diet-induced weight gain in mice

Mammalian target of rapamycin complex 1 (mTORC1) is a major regulator of cell growth and proliferation through fuel sensing. Systemic inhibition of mTOR as well as manipulation of its downstream products prevent diet-induced obesity. The purpose of this study was to determine the consequences of intestine-targeted mTORC1 inhibition. To attenuate intestinal mTORC1 activity, Villin-Cre{sup ER} mice were crossed with Raptor{sup flox/flox} mice, creating an intestinal-specific Raptor null line (i-Raptor −/−). Mice were fed a high fat diet (HFD) and compositional changes as well as food intake levels were assessed. Over a five-week time course, i-Raptor −/− mice consistently gained less body weight on a HFD compared to wildtype (WT) mice secondary to significantly reduced food intake. Importantly, the i-Raptor −/− mice did not appear to be malnourished, demonstrated by their preservation of lean body mass. i-Raptor −/− mice also maintained a normal metabolic profile without significant changes in triglyceride or fasting glucose levels. Further investigation revealed that GDF-15 mRNA expression was significantly enhanced in i-Raptor −/− enterocytes when refed with HFD after overnight starvation. In summary, our study establishes that loss of intestinal specific-mTORC1 is protective of the development of diet-induced obesity by reducing food intake without altering the metabolic profile.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Compound D159687, a phosphodiesterase 4D inhibitor, induces weight and fat mass loss in aged mice without changing lean mass, physical and cognitive function

Highlights: • Seven weeks of Compound D159687 (D159687) induces weight loss in aged mice. • D159687 causes a selective loss of fat mass while preserving lean mass. • The weight loss in D159687 treated mice occurred despite increased food intake. Therapies that recapitulate the health benefits of caloric restriction in older adults are needed. Phosphodiesterase 4 inhibitors demonstrate such promise. We examined their effects on body weight and composition, physical and cognitive function in aged mice using Compound D159687 (D159687).

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Selective synthesis of human milk fat-style structured triglycerides from microalgal oil in a microfluidic reactor packed with immobilized lipase

Human milk fat-style structured triacylglycerols were produced from microalgal oil in a continuous microfluidic reactor packed with immobilized lipase for the first time. A remarkably high conversion efficiency was demonstrated in the microreactor with reaction time being reduced by 8 times, Michaelis constant decreased 10 times, the lipase reuse times increased 2.25-fold compared to those in a batch reactor. In addition, the content of palmitic acid at sn-2 position (89.0%) and polyunsaturated fatty acids at sn-1, 3 positions (81.3%) are slightly improved compared to the product in a batch reactor. The increase of melting points (1.7 °C) and decrease of crystallizing point (3 °C) implied higher quality product was produced using the microfluidic technology. The main cost can be reduced from 212.3 to 14.6 per batch with the microreactor. Altogether, the microfluidic bioconversion technology is promising for modified functional lipids production allowing for cost-effective approach to produce high-value microalgal coproducts.

09 BIOMASS FUELS↗
DOE OSTI2016

Curcumin rescues high fat diet-induced obesity and insulin sensitivity in mice through regulating SREBP pathway

Obesity and its major co-morbidity, type 2 diabetes, have reached an alarming epidemic prevalence without an effective treatment available. It has been demonstrated that inhibition of SREBP pathway may be a useful strategy to treat obesity with type 2 diabetes. Sterol regulatory element-binding proteins (SREBPs) are major transcription factors regulating the expression of genes involved in biosynthesis of cholesterol, fatty acid and triglyceride. In current study, we identified a small molecule, curcumin, inhibited the SREBP expression in vitro. The inhibition of SREBP by curcumin decreased the biosynthesis of cholesterol and fatty acid. In vivo, curcumin ameliorated HFD-induced body weight gain and fat accumulation in liver or adipose tissues, and improved serum lipid levels and insulin sensitivity in HFD-induced obese mice. Consistently, curcumin regulates SREBPs target genes and metabolism associated genes in liver or adipose tissues, which may directly contribute to the lower lipid level and improvement of insulin resistance. Take together, curcumin, a major active component of Curcuma longa could be a potential leading compound for development of drugs for the prevention of obesity and insulin resistance. - Highlights: • Curcumin decreases biosynthesis of cholesterol and fatty acid in vitro. • Curcumin as a SREBP inhibitor ameliorates HFD-induced obesity. • Curcumin as a SREBP inhibitor improves insulin resistance.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

A mouse model of pre-pregnancy maternal obesity combined with offspring exposure to a high-fat diet resulted in cognitive impairment in male offspring

Cognitive impairment is a brain dysfunction characterized by neuropsychological deficits in attention, working memory, and executive function. Maternal obesity and consumption of a high-fat diet (HFD) in the offspring has been suggested to have detrimental consequences for offspring cognitive function through its effect on the hippocampus and prefrontal cortex. Therefore, our study aimed to investigate the effects of maternal obesity and offspring HFD exposure on the brain metabolome of the offspring.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2022

Morphine and high-fat diet differentially alter the gut microbiota composition and metabolic function in lean versus obese mice

There are known associations between opioids, obesity, and the gut microbiome, but the molecular connection/mediation of these relationships is not understood. To better clarify the interplay of physiological, genetic, and microbial factors, this study investigated the microbiome and host inflammatory responses to chronic opioid administration in genetically obese, diet-induced obese, and lean mice. Samples of feces, urine, colon tissue, and plasma were analyzed using targeted LC-MS/MS quantification of metabolites, immunoassays of inflammatory cytokine levels, genome-resolved metagenomics, and metaproteomics. Genetic obesity, diet-induced obesity, and morphine treatment in lean mice each showed increases in distinct inflammatory cytokines. Metagenomic assembly and binning uncovered over 400 novel gut bacterial genomes and species. Morphine administration impacted the microbiome’s composition and function, with the strongest effect observed in lean mice. This microbiome effect was less pronounced than either diet or genetically driven obesity. Based on inferred microbial physiology from the metaproteome datasets, a high-fat diet transitioned constituent microbes away from harvesting diet-derived nutrients and towards nutrients present in the host mucosal layer. Considered together, these results identified novel host-dependent phenotypes, differentiated the effects of genetic obesity versus diet induced obesity on gut microbiome composition and function, and showed that chronic morphine administration altered the gut microbiome.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Rapid Prediction of Low (<1%) trans Fat Content in Edible Oils and Fast Food Lipid Extracts by Infrared Spectroscopy and Partial Least Squares Regression

Abstract The United States Food and Drug Administration (FDA) ruled that partially hydrogenated oils (PHO), the major dietary source of industrially produced trans fat (TF), were no longer “generally recognized as safe (GRAS)” for any use in human food. Consequently, the objective of this study was to develop a rapid screening procedure using attenuated total reflection Fourier‐transform infrared (ATR‐FTIR) spectroscopy in conjunction with partial least squares regression (PLSR) for the quantitative and accurate prediction of low concentrations of trans fatty acid (TFAs) (<1% of total fatty acids (FAs)). Broad‐based calibration models were developed for a combined set of samples consisting of edible oils and fast food lipid extracts. Predicted concentrations of TFAs in the two matrices showed good correlation with the primary reference data generated by gas chromatography (GC) ( R 2 > 0.99) and high accuracy as evidenced by low root‐mean‐square error of cross‐validation (RMSECV) values. The lowest TFA concentration, determined by GC to be 0.13% of total FAs, was accurately predicted by ATR‐FTIR/PLSR as 0.18% of total FAs. This simple, rapid ATR‐FTIR/PLSR methodology has the potential for use as a screening alternative to conventional gas chromatographic methods for predicting the TFA content of edible oils and food lipid extracts for regulatory purposes and quality control of raw material and processed food. Practical Applications F DA ruled that partially hydrogenated oils were no longer “generally recognized as safe (GRAS)” for any use in human food. Consequently, we have proposed a rapid screening procedure, based on infrared spectroscopy and chemometrics, to rapidly and accurately predict low concentrations of trans fatty acids (<1% of total fatty acids) in edible oils and food lipid extracts.

Karunathilaka, Sanjeewa R.↗
DOE OSTI2020

Estimation of Body Fat Percentage for Clinical Pharmacokinetic Studies in Children

Obesity is a prevalent childhood condition and the degree of adiposity appears likely to be an important covariate in the pharmacokinetics (PKs) of many drugs. We undertook these studies to facilitate the evaluation and, where appropriate, quantification of the covariate effect of body fat percentage (BF%) on PK parameters in children. We examined two large databases to determine the values and variabilities of BF% in children with healthy body weights and in those with obesity, comparing the accuracy and precision of BF% estimation by both clinical methods and demographically derived techniques. Additionally, we conducted simulation studies to evaluate the utility of the several methods for application in clinical trials. BF% was correlated with body mass index (BMI), but was highly variable among both children with healthy body weights and those with obesity. Bio‐impedance and several demographically derived techniques produced mean estimates of BF% that differed from dual x‐ray absorptiometry by < 1% (accuracy) and a SD of 5% or less (precision). Simulation studies confirmed that when the differences in precision among the several methods were small compared with unexplained between‐subject variability of a PK parameter, the techniques were of similar value in assessing the contribution of BF%, if any, as a covariate for that PK parameter. The combination of sex and obesity stage explained 68% of the variance of BF% with BMI. The estimation of BF% from sex and obesity stage can routinely be applied to PK clinical trials to evaluate the contribution of BF% as a potential covariate.

Green, Thomas P.↗