Gynostemma Pentaphyllum Increases Exercise Performance and Alters Mitochondrial Respiration and AMPK in Healthy Males.

This research aimed to determine the effects of Gynostemma pentaphyllum (G. pentaphyllum) on exercise performance, AMP-activated protein kinase (AMPK), and mitochondrial signaling in human muscle. This randomized double-blind placebo control crossover study provided placebo or 450 mg of G. pentaphyllum dried leaf extract equivalent to 2.25 g of dry leaf per day for four weeks to 16 healthy untrained young males, separated by four weeks wash-out. Following 4-week supplementation with G. pentaphyllum, participants had significantly lower leptin and blood glucose levels and improved time trial performance over 20 km, which corresponded with a higher muscle oxygen flux compared to placebo. Muscle AMPK Thr172 phosphorylation significantly increased after 60 min exercise following G. pentaphyllum supplementation. AMPK Thr172 phosphorylation levels relative to total AMPK increased earlier following exercise with G. pentaphyllum compared to placebo. Total ACC-α was lower following G. pentaphyllum supplementation compared to placebo. While further research is warranted, G. pentaphyllum supplementation improved exercise performance in healthy untrained males, which corresponded with improved mitochondrial respiration, altered AMPK and ACC, and decreased plasma leptin and glucose levels.

Intake of polyphenols from cereal foods and colorectal cancer risk in the Melbourne Collaborative Cohort Study.

BACKGROUND: Cereal-derived polyphenols have demonstrated protective mechanisms in colorectal cancer (CRC) models; however, confirmation in human studies is lacking. Therefore, this study examined the association between cereal polyphenol intakes and CRC risk in the Melbourne Collaborative Cohort Study (MCCS), a prospective cohort study in Melbourne, Australia that recruited participants between 1990 and 1994 to investigate diet-disease relationships. METHODS: Using food frequency questionnaire diet data matched to polyphenol data, dietary intakes of alkylresorcinols, phenolic acids, lignans, and total polyphenols from cereals were estimated. Hazard ratios (HRs) and 95% confidence intervals for CRC risk were estimated for quintiles of intake with the lowest quintile as the comparison category, using multivariable adjusted Cox proportional hazards models with age as the time axis adjusted for sex, socio-economic status, alcohol consumption, fibre intake, country of birth, total energy intake, physical activity and smoking status. RESULTS: From 35,245 eligible adults, mean (SD) age 54.7 (8.6) years, mostly female (61%) and Australian-born (69%), there were 1394 incident cases of CRC (946 colon cancers and 448 rectal cancers). Results for total cereal polyphenol intake showed reduced HRs in Q2 (HR: 0.80; 95% CI, 0.68-0.95) and Q4 (HR: 0.75; 95% CI, 0.62-0.90), and similar for phenolic acids. Alkylresorcinol intake showed reduced HR in Q3 (HR: 0.80; 95% CI, 0.67-0.95) and Q4 (HR: 0.79; 95% CI, 0.66-0.95). CONCLUSIONS: Overall, the present study showed little evidence of association between intakes of cereal polyphenols and CRC risk. Future investigations may be useful to understand associations between cereal-derived polyphenols and additional cancers in different populations.

Estimated dietary intake of polyphenols from cereal foods and associated lifestyle and demographic factors in the Melbourne Collaborative Cohort Study.

Cereal foods are consumed globally and are important sources of polyphenols with potential health benefits, yet dietary intakes are unclear. We aimed to calculate the dietary intakes of polyphenols from cereal foods in the Melbourne Collaborative Cohort Study (MCCS), and describe intakes by demographic and lifestyle factors. We estimated intakes of alkylresorcinols, lignans and phenolic acids in n = 39,892 eligible MCCS participants, using baseline dietary data (1990-1994) from a 121-item FFQ containing 17 cereal foods, matched to a polyphenol database developed from published literature and Phenol-Explorer Database. Intakes were estimated within groups according to lifestyle and demographic factors. The median (25th-75th percentile) intake of total polyphenols from cereal foods was 86.9 mg/day (51.4-155.8). The most consumed compounds were phenolic acids, with a median intake of 67.1 mg (39.5-118.8), followed by alkylresorcinols of 19.7 mg (10.8-34.6). Lignans made the smallest contribution of 0.50 mg (0.13-0.87). Higher polyphenol intakes were associated with higher relative socio-economic advantage and prudent lifestyles, including lower body mass index (BMI), non-smoking and higher physical activity scores. The findings based on polyphenol data specifically matched to the FFQ provide new information on intakes of cereal polyphenols, and how they might vary according to lifestyle and demographic factors.

Treatment of Diet-Induced Obese Rats with CB2 Agonist AM1241 or CB2 Antagonist AM630 Reduces Leptin and Alters Thermogenic mRNA in Adipose Tissue.

Diet-induced obesity (DIO) is a contributor to co-morbidities, resulting in alterations in hormones, lipids, and low-grade inflammation, with the cannabinoid type 2 receptor (CB2) contributing to the inflammatory response. The effects of modulating CB2 with pharmacological treatments on inflammation and adaptations to the obese state are not known. Therefore, we aimed to investigate the molecular mechanisms in adipose tissue of CB2 agonism and CB2 antagonism treatment in a DIO model. Male Sprague Dawley rats were placed on a high-fat diet (HFD) (21% fat) for 9 weeks, then received daily intraperitoneal injections with a vehicle, AM630 (0.3 mg/kg), or AM1241 (3 mg/kg), for a further 6 weeks. AM630 or AM1241 treatment in DIO rats did not alter their body weight, food intake, or liver weight, and it had no effect on their numerous circulating cytokines or peri-renal fat pad mass. AM1241 decreased heart weight and BAT weight; both treatments (AM630 or AM1241) decreased plasma leptin levels, while AM630 also decreased plasma ghrelin and GLP-1 levels. Both treatments decreased Adrb3 and TNF-α mRNA levels in eWAT and TNF-α levels in pWAT. AM630 treatment also decreased the mRNA levels of Cnr2, leptin, and Slc2a4 in eWAT. In BAT, both treatments decreased leptin, UCP1, and Slc2a4 mRNA levels, with AM1241 also decreasing Adrb3, IL1ß, and PRDM16 mRNA levels, and AM630 increasing IL6 mRNA levels. In DIO, CB2 agonist and CB2 antagonist treatment reduces circulating leptin in the absence of weight loss and modulates the mRNA responsible for thermogenesis.

Methamphetamine Induces Systemic Inflammation and Anxiety: The Role of the Gut-Immune-Brain Axis.

Methamphetamine (METH) is a highly addictive drug abused by millions of users worldwide, thus becoming a global health concern with limited management options. The inefficiency of existing treatment methods has driven research into understanding the mechanisms underlying METH-induced disorders and finding effective treatments. This study aims to understand the complex interactions of the gastrointestinal-immune-nervous systems following an acute METH dose administration as one of the potential underlying molecular mechanisms concentrating on the impact of METH abuse on gut permeability. Findings showed a decreased expression of tight junction proteins ZO-1 and EpCAm in intestinal tissue and the presence of FABP-1 in sera of METH treated mice suggests intestinal wall disruption. The increased presence of CD45+ immune cells in the intestinal wall further confirms gut wall inflammation/disruption. In the brain, the expression of inflammatory markers Ccl2, Cxcl1, IL-1ß, TMEM119, and the presence of albumin were higher in METH mice compared to shams, suggesting METH-induced blood-brain barrier disruption. In the spleen, cellular and gene changes are also noted. In addition, mice treated with an acute dose of METH showed anxious behavior in dark and light, open field, and elevated maze tests compared to sham controls. The findings on METH-induced inflammation and anxiety may provide opportunities to develop effective treatments for METH addiction in the future.

CB1 Ligand AM251 Induces Weight Loss and Fat Reduction in Addition to Increased Systemic Inflammation in Diet-Induced Obesity.

Diet-induced obesity (DIO) reduces fatty acid oxidation in skeletal muscle and decreases circulating levels of adiponectin. Endocannabinoid signaling is overactive in obesity, with some effects abated by antagonism of cannabinoid receptor 1 (CB1). This research aimed to determine if treatment with the global CB1 antagonist/inverse agonist, AM251, in high-fat diet (HFD) fed rats influenced adiponectin signaling in skeletal muscle and a "browning" of white adipose tissue (WAT) defined by UCP1 expression levels. Male Sprague Dawley rats consumed an HFD (21% fat) for 9 weeks before receiving daily intraperitoneal injections with vehicle or AM251 (3 mg/kg) for 6 weeks. mRNA expression of genes involved in metabolic functions were measured in skeletal muscle and adipose tissue, and blood was harvested for the measurement of hormones and cytokines. Muscle citrate synthase activity was also measured. AM251 treatment decreased fat pad weight (epididymal, peri-renal, brown), and plasma levels of leptin, glucagon, ghrelin, and GLP-1, and increased PAI-1 along with a range of pro-inflammatory and anti-inflammatory cytokines; however, AM251 did not alter plasma adiponectin levels, skeletal muscle citrate synthase activity or mRNA expression of the genes measured in muscle. AM251 treatment had no effect on white fat UCP1 expression levels. AM251 decreased fat pad mass, altered plasma hormone levels, but did not induce browning of WAT defined by UCP1 mRNA levels or alter gene expression in muscle treated acutely with adiponectin, demonstrating the complexity of the endocannabinoid system and metabolism. The CB1 ligand AM251 increased systemic inflammation suggesting limitations on its use in metabolic disorders.

The effect of dietary supplementation with blueberry, cyanidin-3-O-ß-glucoside, yoghurt and its peptides on gene expression associated with glucose metabolism in skeletal muscle obtained from a high-fat-high-carbohydrate diet induced obesity model.

Obesity is a leading global health problem contributing to various chronic diseases, including type II diabetes mellitus (T2DM). The aim of this study was to investigate whether blueberries, yoghurt, and their respective bioactive components, Cyanidin-3-O-ß-glucoside (C3G) and peptides alone or in combinations, alter the expression of genes related to glucose metabolism in skeletal muscles from diet-induced obese mice. In extensor digitorum longus (EDL), yoghurt up-regulated the expression of activation of 5'adenosine monophosphate-activated protein kinase (AMPK), insulin receptor substrate-1 (IRS-1), phosphatidylinositol-3 kinase (PI3K) and glucose transporter 4 (GLUT4), and down-regulated the expression of angiotensin II receptor type 1 (AGTR-1). The combination of blueberries and yoghurt down-regulated the mRNA expression of AGTR-1 and Forkhead box protein O1 (FoxO1) in the EDL. Whereas the combination of C3G and peptides down-regulated AGTR-1 and up-regulated GLUT4 mRNA expression in the EDL. In the soleus, blueberries and yoghurt alone, and their combination down-regulated AGTR-1 and up-regulated GLUT4 mRNA expression. In summary blueberries and yoghurt, regulated multiple genes associated with glucose metabolism in skeletal muscles, and therefore may play a role in the management and prevention of T2DM.

Cisplatin for cancer therapy and overcoming chemoresistance.

Cisplatin spearheads the anticancer chemotherapeutics in present-day use although acute toxicity is its primary impediment factor. Among a plethora of experimental medications, a drug as effective or surpassing the benefits of cisplatin has not been discovered yet. Although Oxaliplatin is considered more superior to cisplatin, the former has been better for colorectal cancer while cisplatin is widely used for treating gynaecological cancers. Carcinoma imposes a heavy toll on mortality rates worldwide despite the novel treatment strategies and detection methods that have been introduced; nanomedicine combined with precision medicine, immunotherapy, volume-regulated anion channels, and fluorodeoxyglucose-positron emission tomography. Millions of deaths occur annually from metastatic cancers which escape early detection and the concomitant diseases caused by highly toxic chemotherapy that causes organ damage. It continues due to insufficient knowledge of the debilitative mechanisms induced by cancer biology. To overcome chemoresistance and to attenuate the adverse effects of cisplatin therapy, both in vitro and in vivo models of cisplatin-treated cancers and a few multi-centred, multi-phasic, randomized clinical trials in pursuant with recent novel strategies have been tested. They include plant-based phytochemical compounds, de novo drug delivery systems, biochemical/immune pathways, 2D and 3D cell culture models using small molecule inhibitors and genetic/epigenetic mechanisms, that have contributed to further the understanding of cisplatin's role in modulating the tumour microenvironment. Cisplatin was beneficial in cancer therapy for modulating the putative cellular mechanisms; apoptosis, autophagy, cell cycle arrest and gene therapy of micro RNAs. Specific importance of drug influx, efflux, systemic circulatory toxicity, half-maximal inhibition, and the augmentation of host immunometabolism have been identified. This review offers a discourse on the recent anti-neoplastic treatment strategies to enhance cisplatin efficacy and to overcome chemoresistance, given its superiority among other tolerable chemotherapies.

Anthocyanins in Chronic Diseases: The Power of Purple.

Anthocyanins are mainly purple-coloured phenolic compounds of plant origin that as secondary metabolites are important in plant survival. Understanding their health benefits in humans requires sourcing these unstable compounds in sufficient quantities at a reasonable cost, which has led to improved methods of extraction. Dark-coloured fruits, cereals and vegetables are current sources of these compounds. The range of potential sustainable sources is much larger and includes non-commercialised native plants from around the world and agri-waste containing anthocyanins. In the last 5 years, there have been significant advances in developing the therapeutic potential of anthocyanins in chronic human diseases. Anthocyanins exert their beneficial effects through improvements in gut microbiota, oxidative stress and inflammation, and modulation of neuropeptides such as insulin-like growth factor-1. Their health benefits in humans include reduced cognitive decline; protection of organs such as the liver, as well as the cardiovascular system, gastrointestinal tract and kidneys; improvements in bone health and obesity; and regulation of glucose and lipid metabolism. This review summarises some of the sources of anthocyanins and their mechanisms and benefits in the treatment of chronic human diseases.

A Pilot Study on the Impact of Menstrual Cycle Phase on Elite Australian Football Athletes.

The effect of the menstrual cycle on athlete performance, wellbeing and perceived exertion and fatigue is not well understood. Furthermore, it has not been investigated specifically in Australian Football athletes. This pilot study aimed to explore how naturally menstruating Australian Football athletes may be affected by menstrual cycle phase. The data collected from the routine monitoring of five naturally menstruating athletes (average menstrual cycle length of 28 ± 3 [SD] days) in one team (athlete age range 18-35 years) competing in the Women's Australian Football League during the 2019 season were retrospectively analysed to compare performance (countermovement jump parameters and adductor squeeze pressure), perceived exertion, perceived fatigue and wellbeing (perceived sleep quality, stress and soreness) outcomes between the follicular and luteal phases. Performance, perceived exertion, stress and soreness did not appear to be affected by menstrual cycle phase (p > 0.17). However, perceived fatigue appeared to be significantly greater (p = 0.042) and sleep quality worse (p = 0.005) in the luteal phase. This pilot study suggests further research focusing on the effect of menstrual cycle phase on subjective fatigue and wellbeing is warranted.

The Role of Atypical Cannabinoid Ligands O-1602 and O-1918 on Skeletal Muscle Homeostasis with a Focus on Obesity.

O-1602 and O-1918 are atypical cannabinoid ligands for GPR55 and GPR18, which may be novel pharmaceuticals for the treatment of obesity by targeting energy homeostasis regulation in skeletal muscle. This study aimed to determine the effect of O-1602 or O-1918 on markers of oxidative capacity and fatty acid metabolism in the skeletal muscle. Diet-induced obese (DIO) male Sprague Dawley rats were administered a daily intraperitoneal injection of O-1602, O-1918 or vehicle for 6 weeks. C2C12 myotubes were treated with O-1602 or O-1918 and human primary myotubes were treated with O-1918. GPR18 mRNA was expressed in the skeletal muscle of DIO rats and was up-regulated in red gastrocnemius when compared with white gastrocnemius. O-1602 had no effect on mRNA expression on selected markers for oxidative capacity, fatty acid metabolism or adiponectin signalling in gastrocnemius from DIO rats or in C2C12 myotubes, while APPL2 mRNA was up-regulated in white gastrocnemius in DIO rats treated with O-1918. In C2C12 myotubes treated with O-1918, PGC1α, NFATc1 and PDK4 mRNA were up-regulated. There were no effects of O-1918 on mRNA expression in human primary myotubes derived from obese and obese T2DM individuals. In conclusion, O-1602 does not alter mRNA expression of key pathways important for skeletal muscle energy homeostasis in obesity. In contrast, O-1918 appears to alter markers of oxidative capacity and fatty acid metabolism in C2C12 myotubes only. GPR18 is expressed in DIO rat skeletal muscle and future work could focus on selectively modulating GPR18 in a tissue-specific manner, which may be beneficial for obesity-targeted therapies.

Pharmacophore Directed Screening of Agonistic Natural Molecules Showing Affinity to 5HT2C Receptor.

Obesity prevalence continues to be a foremost health concern across the globe leading to the development of major health risk conditions like type II diabetes, hyperlipidemia, hypertension and even cancers. Because of the deprived drug-based management system, there is an urgent need for the development of new drugs aiming at satiety and appetite control targets. Among the reported satiety signaling targets, 5HT2C receptor plays a crucial role in decreasing appetite and has become a promising target for the development of anti-obesity drugs. Lorcaserin, a 5HT2C receptor agonist and the only drug available in the market, was designed based on the receptor mechanism of action. Due to limited drug options available and considering the adverse drug effects of Lorcaserin, the development of new drugs which are highly specific toward the 5HT2C target and with lesser side effects is essential. The present study is majorly focused on developing new 5HT2C agonists through computational approaches like screening, docking, and simulation using Phase, QikProp, Glide and Desmond applications of the Schrodinger suite. Screening protocols resulted in eight best hit molecules with affinity for the receptor and among them, five hits displayed binding affinity toward the conserved residue Asp 134 of the receptor. The stability of the five molecules in complex with the 5HT2C receptor was studied through molecular dynamic simulations. Three molecules, ZINC32123870, ZINC40312983 and ZINC32124535, maintained stable interactions with the Asp 134 residue throughout the 50 ns simulation run time. Further, due to the high sequence similarity seen among the receptors of 5HT2 family, the three potential hits were cross validated against other subtypes 5HT2A and 5HT2B of the 5HT2 family to determine the specificity of the molecules against the target. Among the three hits, ZINC32124535 was identified as the best potential hit based on the hydrogen bond interaction percentage with Asp residue [5HT2A (Asp 155:60%); 5HT2B (Asp155: No interaction); 5HT2C (Asp 134:86%)]. The ZINC32124535 molecule produced one salt bridge and hydrogen bond interactions with Asp 134, alike the known drug Lorcaserin. Based on the results, ZINC32124535 was identified as the best potential hit against the 5HT2C receptor.

Atypical cannabinoid ligands O-1602 and O-1918 administered chronically in diet-induced obesity.

Atypical cannabinoid compounds O-1602 and O-1918 are ligands for the putative cannabinoid receptors G protein-coupled receptor 55 and G protein-coupled receptor 18. The role of O-1602 and O-1918 in attenuating obesity and obesity-related pathologies is unknown. Therefore, we aimed to determine the role that either compound had on body weight and body composition, renal and hepatic function in diet-induced obesity. Male Sprague-Dawley rats were fed a high-fat diet (40% digestible energy from lipids) or a standard chow diet for 10 weeks. In a separate cohort, male Sprague-Dawley rats were fed a high-fat diet for 9 weeks and then injected daily with 5 mg/kg O-1602, 1 mg/kg O-1918 or vehicle (0.9% saline/0.75% Tween 80) for a further 6 weeks. Our data demonstrated that high-fat feeding upregulates whole kidney G protein receptor 55 expression. In diet-induced obesity, we also demonstrated O-1602 reduces body weight, body fat and improves albuminuria. Despite this, treatment with O-1602 resulted in gross morphological changes in the liver and kidney. Treatment with O-1918 improved albuminuria, but did not alter body weight or fat composition. In addition, treatment with O-1918 also upregulated circulation of pro-inflammatory cytokines including IL-1α, IL-2, IL-17α, IL-18 and RANTES as well as plasma AST. Thus O-1602 and O-1918 appear not to be suitable treatments for obesity and related comorbidities, due to their effects on organ morphology and pro-inflammatory signaling in obesity.

Caralluma fimbriata extract activity involves the 5-HT2c receptor in PWS Snord116 deletion mouse model.

INTRODUCTION: In Prader-Willi syndrome (PWS), nonprotein coding small nucleolar (sno) RNAs are involved in the paternally deleted region of chromosome 15q11.2-q13, which is believed to cause the hyperphagic phenotype of PWS. Central to this is SnoRNA116. The supplement Caralluma fimbriata extract (CFE) has been shown to decrease appetite behavior in some individuals with PWS. We therefore investigated the mechanism underpinning the effect of CFE on food intake in the Snord116del mouse. Experiments utilized appetite stimulants which included a 5-hydroxytryptamine (5-HT) 2c receptor antagonist (SB242084), as the 5-HT2cR is implicated in central signaling of satiety. METHODS: After 9-week chronic CFE treatment (33 mg or 100 mg kg-1  day-1 ) or placebo, the 14-week-old Snord116del (SNO) and wild-type mice (n = 72) were rotated through intraperitoneal injections of (a) isotonic saline; (b) 400 mg/kg of 2-deoxyglucose (2DG) (glucose deprivation); (c) 100 mglkg beta-mercaptoacetate (MA), fatty acid signaling; and (d) SB242084 (a selective 5HT2cR antagonist), with 5 days between reagents. Assessments of food intake were from baseline to 4 hr, followed by immunohistochemistry of neural activity utilizing c-Fos, neuropeptide Y, and alpha-melanocyte-stimulating hormone within hypothalamic appetite pathways. RESULTS: Caralluma fimbriata extract administration decreased food intake more strongly in the SNO100CFE group with significantly stimulated food intake demonstrated during coadministration with SB242084. Though stimulatory deprivation was expected to stimulate food intake, 2DG and MA resulted in lower intake in the snord116del mice compared to the WT animals (p = <0.001). Immunohistochemical mapping of hypothalamic neural activity was consistent with the behavioral studies. CONCLUSIONS: This study identifies a role for the 5-HT2cR in CFE-induced appetite suppression and significant stimulatory feeding disruptions in the snord116del mouse model.

The Acute Effect of Oleic- or Linoleic Acid-Containing Meals on Appetite and Metabolic Markers; A Pilot Study in Overweight or Obese Individuals.

Despite the abundance of plant-derived fats in our diet, their effects on appetite, and metabolic markers, remain unclear. This single-blinded 3-way cross-over pilot study aimed to investigate the ability of the two most abundant dietary plant-derived fats, oleic (OA) and linoleic (LA) acids, to modulate postprandial appetite and levels of circulating appetite and metabolic regulators in overweight/obese individuals. Meals were a high-carbohydrate control, a high-OA or a high-LA meal, and provided 30% of participants' estimated energy requirements. Meals were consumed after an overnight fast, with blood samples collected over 3» h. Appetite parameters were assessed via a validated visual analogue scale questionnaire. Hormones and other circulating factors were quantified using multiplex immunoassays. Eight participants (age 45.8 ± 3.6 (years), body mass index 32.0 ± 1.3 (kg/m²)) completed the study. All meals significantly increased fullness and reduced desire to eat. The control and high-OA meals significantly decreased prospective food intake. The high-LA meal increased ghrelin levels (p < 0.05), a hormone which encourages food intake. This was coupled with a significant acute increase in resistin levels, which impairs insulin signaling. Taken together, this study indicates that in overweight/obese individuals, high-LA meals may promote excess energy intake and alter glucose handling, though a larger cohort may be required to strengthen results.

Anaphylaxis to packaged foods in Australasia.

AIMS: To examine reports of anaphylaxis in Australasia from consumption of packaged food products with or without precautionary allergen labelling (PAL), where the known allergen triggers were not a listed ingredient. METHODS: A questionnaire was sent to all members of the Australasian Society of Clinical Immunology and Allergy (n = 548). Participants were asked to complete a survey reporting whether they have had seen any patients over the last 3 months reporting anaphylaxis following ingestion of a packaged food where the suspected food allergen was not a listed ingredient. RESULTS: Of the n = 548 members approached, n = 198 responded (response rate 36.1%).There were 14 reports of anaphylaxis to packaged foods (where the suspected allergen was not a listed ingredient), which met the case definition from a total of 198 respondents over the 9-month period. Of those reactions, 50.0% (confidence interval 95% 21-78) were reported from foods that did not have a PAL statement, and 50.0% (confidence interval 95% 21-78) were due to peanuts. CONCLUSION: Anaphylaxis to undeclared allergens was not rare and did not appear to depend on whether the product was labelled with precautionary advice. There is currently no reliable labelling system that can inform food-allergic consumers of safer food choices. Improvements in the regulation of food labelling with PAL are required.

Are food allergic consumers ready for informative precautionary allergen labelling?

Precautionary allergen labelling (PAL) has resulted in consumer confusion. Previous research has shown that interpretive labels (using graphics, symbols, or colours) are better understood than the traditional forms of labels. In this study, we aimed to understand if consumers would use interpretive labels (symbol, mobile phone application and a toll-free number) with or without medical advice that was advocated by the food industry rather than the normal PAL. This is relevant information for industry and clinicians as it provides an insight into the food allergic perception regarding PAL.

Beetroot and Sodium Nitrate Ameliorate Cardiometabolic Changes in Diet-Induced Obese Hypertensive Rats.

SCOPE: Dietary intake of beetroot by humans reduces blood pressure but whether this is caused by nitrate or betanin is not well-defined; neither are effects on other signs of metabolic syndrome. METHODS AND RESULTS: Rats fed a high-carbohydrate, high-fat diet (H) for 16 weeks developed abdominal obesity, hypertension, altered cardiovascular and liver structure and function, and impaired glucose tolerance compared to rats fed a corn starch diet (C). H rats treated with ∼16 mg/kg/day of nitrate either from beetroot juice (H+B) or sodium nitrate (H+N) for the last 8 weeks reduced systolic blood pressure by ∼25 mmHg, improved cardiac structure and function, plasma lipid profile and plasma markers of liver function, reduced inflammatory cell infiltration in heart and liver and decreased left ventricular fibrosis. In the left ventricle, H rats increased mRNA expression of connective tissue growth factor (CTGF), monocyte chemoattractant protein 1 (MCP-1), matrix metalloproteinase-2 (MMP-2), and adenosine monophosphate-activated protein kinase-alpha (AMPK-α) and decreased mRNA expression of peroxisome proliferator-activated receptor-alpha (PPAR-α); both beetroot and sodium nitrate diet-fed rats decreased CTGF threefold, MCP-1, and MMP-2 twofold, and doubled PPAR-α mRNA expression in left ventricular tissue. CONCLUSION: The similar functional and molecular responses to beetroot and sodium nitrate indicate that the nitrate content of beetroot reduced inflammation and improved cardiovascular, liver, and metabolic function in rats with metabolic syndrome, rather than betanin.