Physiol Endocrinol Metab Research Articles

Neuronostatin accts as a counterregulatory factor to protect against hypoglycemia

Neuronostatin (NST) is a 13-amino acid hormone derived from the somatostatin (SST) preprohormone that exerts metabolic and cardiovascular actions in many tissue types. In transformed alpha cell lines and isolated rat islets neuronostatin enhanced low glucose-stimulated proglucagon transcription and glucagon secretion1. Additionally, neuronostatin inhibited high glucose-stimulated insulin secretion from isolated rat islets, which was mirrored in vivo in rats subjected to an intra-arterial glucose tolerance test. Rats that received a bolus injection of neuronostatin followed by infusion glucose exhibited delayed glucose disposal and impaired insulin release, causing an increased peak blood glucose1. We, therefore hypothesized the ability of neuronostatin to act as a counterregularoty factor to protect against hypoglycemia. We found that Neuronostatin administered prior to an insulin tolerance test significantly reduced hypoglycemia compared to the saline control. In addition, we found that administration of exogenous Insulin significantly reduced Neuronostatin plasma levels. These data suggest Neuronostatin may act as a counterregulatory factor in adult, male rats to prevent hypoglycemia. However, after menopause or OVX, a precipitous decline in insulin sensitivity parallels an increase in fat mass, suggesting estrogens at physiological concentrations may maintain insulin action and glucose tolerance. We therefore investigated the neuronostatin-induced blood glucose changes in conscious, cycling females. We found blood glucose levels following neuronostatin administration decreased on diestrus, when both estrogen and progesterone levels are low, but not on proestrus or estrus. From these data we conclude that the metabolic actions of Neuronostatin are modulated by sex hormone status. Further studies are required to determine the contributions of chromosomal sex and individual sex hormones to these metabolic effects of Neuronostatin.1. Salvatori AS, Elrick MM, Samson WK, Corbett JA, Yosten GL. Neuronostatin inhibits glucose-stimulated insulin secretion via direct action on the pancreatic alpha-cell. Am J Physiol Endocrinol Metab. 2014;306:E1257–E1263. Saint Louis University Internal Funds This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Effect of caffeine on mitochondrial biogenesis in the skeletal muscle - A narrative review.

Caffeine is one of the most widely used substances as recreational drug for performance-enhancement in sport, underpinned by a strong evidence base. Although the effects of caffeine are widely investigated within the scope of performance physiology, the molecular effects of caffeine within skeletal muscle remain unclear. Evidence from invitro and invivo models suggest that caffeine regulates the glucose metabolism in the skeletal muscle. Moreover, caffeine seems to stimulate CaMKII, PPARδ/β, AMPK and PGC1α, classical markers of exercise-adaptations, including mitochondrial biogenesis and mitochondrial content. This review summarizes evidence to suggest caffeine-effects within skeletal muscle fibers, focusing on the putative role of caffeine on mitochondrial biogenesis to explore whether caffeine supplementation might be a strategy to enhance mitochondrial biogenesis.

Retraction for Jiang et al., volume 304, 2012, p. E74-E86.

RetractionRetraction for Jiang et al., volume 304, 2012, p. E74–E86Published Online:11 Oct 2022https://doi.org/10.1152/ajpendo.00176.2012_retRetracted articleMoreSectionsPDF (98 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Jiang S, Guo R, Zhang Y, Zou Y, Ren J. Heavy metal scavenger metallothionein mitigates deep hypothermia-induced myocardial contractile anomalies: role of autophagy. Am J Physiol Endocrinol Metab 304: E74–E86, 2009. First published November 6, 2012. doi: 10.1152/ajpendo.00176.2012.The American Physiological Society is issuing a retraction of this article at the request of the University of Wyoming. An investigation uncovered evidence of imaging reuse and manipulation in Fig. 3 that significantly affect the results and conclusions reported in the manuscript.This article has no references to display. Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationRelated ArticlesHeavy metal scavenger metallothionein mitigates deep hypothermia-induced myocardial contractile anomalies: role of autophagy 01 Jan 2013American Journal of Physiology-Endocrinology and Metabolism More from this issue > Volume 323Issue 4October 2022Pages E402-E402 Crossmark Copyright & PermissionsCopyright © 2022 the American Physiological Society.https://doi.org/10.1152/ajpendo.00176.2012_retPubMed36219584History Published online 11 October 2022 Published in print 1 October 2022 Metrics

Alcohol exacerbated biochemical and biophysical alterations in liver mitochondrial membrane of diabetic male wistar rats – A possible amelioration by green tea

Alcohol exacerbated biochemical and biophysical alterations in liver mitochondrial membrane of diabetic male wistar rats – A possible amelioration by green tea

The Glucagon-Like Peptide 1 Receptor Agonist Liraglutide Stimulates Mechanistic Target of Rapamycin (mTOR) Signaling via PKA And Akt

Glucagon-like peptide 1 receptor (GLP-1R) agonists enhance glucose-stimulated insulin secretion and act on several regions of the brain to reduce food intake and body weight, making the GLP-1R a major therapeutic target for the treatment of type 2 diabetes and obesity. Surprisingly, little is known about the signaling mechanisms mediating the food intake-lowering effects of GLP-1R agonists. We have previously shown that inhibiting the mechanistic Target of Rapamycin (mTOR) in the ventromedial hypothalamus blocks anorexia induced by GLP-1R activation in this brain nucleus (1). Therefore, the goal of the present studies is to elucidate the mechanisms by which GLP-1R activation stimulates mTOR signaling. To accomplish this, we treated Chinese Hamster Ovary cells stably expressing the human GLP-1R with the GLP-1R agonist liraglutide (Lira) in combination with inhibitors of various signaling molecules. Since PKA is a canonical target of GLP-1R signaling, and PKA phosphorylates mTOR and its regulating protein Raptor following β-adrenergic stimulation (2), we used the PKA inhibitors H89 and KT 5720 to examine whether PKA is required for the stimulation of mTOR activity by Lira. We expressed myc-tagged mTOR or Raptor in GLP-1R stably expressing CHO cells, treated them with Lira, immunoprecipitated myc-mTOR or myc-Raptor, and immunoblotted for the PKA substrate RRXS/T motif. We found that Lira significantly increased PKA-substrate motif phosphorylation of myc-Raptor but not myc-mTOR, and this was blocked by pre-treatment with H89. Lira also failed to stimulate phosphorylation of a Ser791Ala Raptor mutant that cannot be phosphorylated by PKA (2). To test whether Akt, a well-known regulator of mTOR activity, contributes to the activation of mTOR signaling by Lira, we pre-treated GLP-1R stably expressing CHO cells with either of the Akt inhibitors Akt-i 1/2 and MK-2206 followed by treatment with Lira or forskolin (Fsk), a cAMP inducer and PKA activator. Pre-treatment with either Akt-i 1/2 or MK-2206 blocked mTOR activation by both Lira and Fsk. This suggests that the contribution of Akt to Lira-induced mTOR activation is likely downstream of cAMP production. Taken together, our results suggest a novel two-pronged, PKA-dependent mechanism for the stimulation of mTOR signaling following GLP-1R activation – directly via phosphorylation of Raptor and indirectly via stimulation of Akt. Future studies will assess the respective contributions and temporal dynamics of each of these pathways. Reference: (1) Burmeister et al., Am J Physiol Endocrinol Metab. 2017 Aug;313: E651–E662. (2) Liu et al., J Clin Invest. 2016;126(5):1704-1716.

The Association between Dietary Inflammatory Index and Sex Hormones among Men in the United States.

This study investigated the association between Dietary Inflammatory Index and sex hormones in a large, nationally representative adult male sample. We utilized data from the 2013-2014 and 2015-2016 National Health and Nutrition Examination Survey. Males aged ≥20 years who provided a 24-hour dietary intake history and underwent serum sex hormone testing were included in analysis. Weighted proportions and multivariable analysis controlling for age, race, energy, smoking status, education level, body mass index and time of venipuncture were used to evaluate the associations between Dietary Inflammatory Index and sex hormones. For 4,151 participants, Dietary Inflammatory Index ranged from -5.05 to 5.48. Mean±SD total testosterone was 419.30±176.27 ng/dl. Mean±SD total testosterone was lower among men in the highest tertile compared with men in the lowest tertile group (410.42±171.97 vs 422.71±175.69, p <0.001). A per unit increase in Dietary Inflammatory Index was related to 4.0% (95% CI 0.5-7.6) higher odds of testosterone deficiency. In the fully adjusted multivariable model, males in Dietary Inflammatory Index tertile 3 (the most pro-inflammatory) had 29.6% (3.1-63.0) higher odds of testosterone deficiency than those in tertile 1 (p trend=0.025). Interaction tests revealed no significant effect of body mass index on the association of Dietary Inflammatory Index with testosterone deficiency and all sex hormone parameters. Men adhering to a more pro-inflammatory diet appear to have a higher risk of testosterone deficiency, indicating the important role of diet in male reproductive health.

Understanding the effects of nutrition and post-exercise nutrition on skeletal muscle protein turnover: Insights from stable isotope studies

Understanding the effects of nutrition and post-exercise nutrition on skeletal muscle protein turnover: Insights from stable isotope studies

Reply to Jakovac: “COVID-19 and vitamin D—Is there a link and an opportunity for intervention?”

Reply to Jakovac: “COVID-19 and vitamin D—Is there a link and an opportunity for intervention?”

Consideration of Pannexin 1 channels in COVID-19 pathology and treatment.

Pannexin1 (PANX1) is a ubiquitously expressed, channel-forming protein found in a number of tissues thoughout the body (e.g. lung, vasculature, liver, central nervous system, immune system) that is important in many key physiological and immune responses. PANX1 channels passively flux ATP (predominantly), multiple metabolites, and likely other small anions. PANX1 channels regulate inflammation and host responses to several pathogens, including viruses. While there is currently no evidence suggesting novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and PANX1 directly interact, there is an urgent need for therapeutic strategies, especially those targeting the hyper-inflammation and cytokine storm that occurs in severe cases of COVID-19. Here we argue that PANX1, and drugs known to target PANX1 (including the FDA-approved drug probenecid), should be the focus of further investigation in the context of SARS-CoV-2 infection and its associated pathology in COVID-19 patients.

Reply to Jakovac: About COVID-19 and vitamin D

Reply to Jakovac: About COVID-19 and vitamin D

MON-010 Effects of Delta-9-Tetrahydrocannabinol (THC) on Oocyte Competence and Early Embryonic Development

Cannabis is the highest used recreational drug amongst individuals of reproductive age. Fertility clinics advise against cannabis use when undergoing fertility treatments, but the literature backing this statement is weak. This rise in cannabis use has occurred simultaneously with the increase in the percentage of the main psychoactive component of cannabis, delta-9 tetrahydrocannabinol (THC) (1). Current literature suggests that THC mimics the effects of endogenous cannabinoids, binding to cannabinoid receptor 1 (CB1), which has been identified in reproductive tissues (2).Our research aims to study the impact of THC on oocyte maturation and pre-implantation embryonic development. An in vitro bovine system was used as it is the most appropriate translational model to humans for in vitro reproductive toxicity studies. Bovine oocytes were collected and matured under five treatment groups: control, vehicle (1:1:18 ethanol: TWEEN: saline), low THC (0.032uM), mid THC (0.32uM) and high THC (3.2uM). These doses mimic plasma concentrations reached after therapeutic (0.032uM) or low/high recreational (0.32uM and 3.2uM) cannabis use (3). We hypothesise that THC affects oocyte competence and proper early embryonic development in vitro.A negative THC dose-dependent response in cleavage rate was observed, with the highest THC group cleaving at 70.2% rate compared to 86.8% and 85.5% of control and vehicle groups, respectively (p<0.0001, n=7). There was no significant difference in blastocyst rate, suggesting that oocyte THC exposure affects the numbers of oocytes capable of development, but those able to cleave will properly reach blastocyst stage. We analyzed changes in gene expression, i) by a full RNA transcriptome analysis (24,128 transcripts screened) and ii) by quantification of Connexin 37 (CX37) and 43 (CX43) mRNA levels. Connexin expression is correlated to oocyte competence (4). RNA transcriptome analysis showed 62 genes that were significantly downregulated only in the low THC group. CX mRNA levels were measured via droplet digital PCR in both cumulus-oocyte complexes (COCs) and blastocysts. No significant differences were detected in blastocysts, however, a significant decrease in both CX37 and CX43 levels was measured in the low THC group in COCs (p<0.05, n= 9). Differences seen exclusively at the low THC dose suggest a role of THC as partial agonist of CB1.This research aims to understand the effects of cannabis on fertility, as current knowledge during pre-implantation development is limited, making it difficult for physicians to properly advise patients undergoing IVF. Reference: (1) ElSohly et al., Biol Psychiatry. 2016 Apr 1;79(7):613–9. (2) El-Talatini et al., PLoS ONE. 2009 Feb 24;4(2):e4579. (3) Whan et al., Fertil Steril. 2006 Mar;85(3):653–60. (4) Wang et al., Am J Physiol Endocrinol Metab. 2012 Jun 15;302(12):1511–8

AJP-Regulatory, Integrative and Comparative Physiology: Looking Toward the Future

<i>AJP-Regulatory, Integrative and Comparative Physiology</i>: Looking Toward the Future

In memory of Michelle Lane: 1970 - 2020.

In memory of Michelle Lane: 1970 - 2020.

It's well and truly time to stop stating that AMPK regulates glucose uptake and fat oxidation during exercise.

None for Perspective.

Fetal androgen signaling defects affect pancreatic β-cell mass and function, leading to glucose intolerance in high-fat diet-fed male rats.

We previously demonstrated that androgen signaling expands pancreatic β-cell mass in the sexual maturation period (Am J Physiol Endocrinol Metab 314: E274-E286, 2018). The aim of this study was to elucidate whether fetal androgen signaling plays important roles in β-cell mass development and β-cell function in adulthood, defects of which are associated with type 2 diabetes mellitus. In the pancreas of male fetuses, androgen receptor (AR) was strongly expressed in the cytoplasm and at the cell membrane of Nkx6.1-positive β-cell precursor cells but was markedly reduced in insulin-positive β-cells. Administration of the anti-androgen flutamide to pregnant dams during late gestation reduced β-cell mass and Ki67-positive proliferating β-cells at birth in a male-specific manner without affecting body weight. The decrease of β-cell mass in flutamide-exposed male rats was not recovered when rats were fed a standard diet, whereas it was fully recovered when rats were fed a high-fat diet (HFD), at 6 and 12 wk of age. Flutamide exposure in utero led to the development of glucose intolerance in male rats due to a decrease in insulin secretion when fed HFD but not standard diet. Insulin sensitivity did not differ between the two groups irrespective of diet. These results indicated that the action of fetal androgen contributed to β-cell mass expansion in a sex-specific manner at birth and to the development of glucose intolerance by decreasing the secretion of insulin in HFD-fed male rats. Our data demonstrated the involvement of fetal androgen signaling in hypothesized sex differences in the developmental origins of health and disease by affecting pancreatic β-cell function.

Acute behavioural and physiological responses of sheep to S/C ivermectin injection

Acute behavioural and physiological responses of sheep to S/C ivermectin injection

CORRIGENDUM.

CorrigendumCORRIGENDUMPublished Online:05 Feb 2019https://doi.org/10.1152/ajpendo.zh1-8043-corr.2019Original articleMoreSectionsPDF (28 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Kulas JA, Franklin WF, Smith NA, Manocha GD, Puig KL, Nagamoto-Combs K, Hendrix RD, Taglialatela G, Barger SW, Combs CK. Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues. Am J Physiol Endocrinol Metab 316: E106–E120, 2019. First published November 13, 2018; doi:10.1152/ajpendo.00279.2018.—In disclosures, the following statement was omitted in error: “S. W. Barger receives royalties from Merck/Sigma-Aldrich for the sales of secreted amyloid precursor protein.”This article has no references to display. Download PDF Previous Back to Top FiguresReferencesRelatedInformation Related ArticlesAblation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues 05 Jan 2019American Journal of Physiology-Endocrinology and Metabolism More from this issue > Volume 316Issue 2February 2019Pages E345-E345 Copyright & PermissionsCopyright © 2019 the American Physiological Societyhttps://doi.org/10.1152/ajpendo.zh1-8043-corr.2019PubMed30721099History Published online 5 February 2019 Published in print 1 February 2019 Metrics

ETHANOLIC EXTRACT OF TUBTIM-CHUMPHAE RICE BRAN DECREASES INSULIN RESISTANCE AND INTRAHEPATIC FAT ACCUMULATION IN HIGH-FAT-HIGH-FRUCTOSE DIET FED RATS

Objective: Tubtim-chumphae rice is hybrid Thai rice with a red pericarp. This study was aimed to investigate the effect of Tubtim-chumphae rice bran on insulin resistance and intrahepatic fat accumulation in high-fat-high-fructose diet (HFFD) fed rats.Methods: Ethanolic extract of rice bran (ERB) was prepared using a 50% ethanol-water. Male Sprague-Dawley rats were fed HFFD (40% lard, 20% fructose) for 10 weeks, followed by concomitant administrations of distilled water or ERB at 250 or 500 mg/kg/day or pioglitazone at 10 mg/kg/day for a further 4 weeks in treated groups. Normal control rats were fed normal chow and distilled water. At the end of all treatments, fasting blood glucose (FBG), an oral glucose tolerance test (OGTT), serum insulin levels, lipid profiles, and liver fat contents were measured. Liver histological and peroxisome proliferator-activated receptor-α (PPAR-α) gene expression examinations were performed.Results: At week 14, control HFFD rats had significantly (p&lt;0.05) higher FBG, low-density lipoprotein cholesterol, triglycerides, and insulin secretions together with impaired OGTT as compared to normal control rats. These parameters indicated an insulin resistant and dyslipidemic condition in HFFD rats. ERB 250 and 500 mg/kg or pioglitazone 10 mg/kg significantly ameliorated all of these changes. HFFD also caused a significant increase in fat accumulation and a decrease in PPAR-α gene expression in the livers which were significantly decreased by ERB.Conclusions: ERB decreases insulin resistance and intrahepatic fat accumulation possibly through increasing PPAR-α gene expression in HFFD rats. ERB might possibly be a neutraceutical for the metabolic syndrome patients.1. Gauthier MS, Favier R, Lavoie JM. Time course of the development of non-alcoholic hepatic steatosis in response to high-fat diet-induced obesity in rats. Br J Nutr 2006;95:273-81.2. Roberts CK, Hevener AL, Barnard RJ. Metabolic syndrome and insulin resistance: Underlying causes and modification by exercise training. Compr Physiol 2013;3:1-58.3. Grundy SM. Metabolic syndrome update. Trends Cardiovasc Med 2016;26:364-73.4. Fouret G, Gaillet S, Lecomte J, Bonafos B, Djohan F, Barea B, et al. 20-week follow-up of hepatic steatosis installation and liver mitochondrial structure and activity and their interrelation in rats fed a high-fat-high-fructose diet. Br J Nutr 2018;119:368-80.5. Dekker MJ, Su Q, Baker C, Rutledge AC, Adeli K. Fructose: A highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome. Am J Physiol Endocrinol Metab 2010;299:E685-94.6. Vichit W, Saewan N. Antioxidant activities and cytotoxicity of thai pigmented rice. Int J Pharm Pharm Sci 2015;7:329-34.7. Settharaksa S, Madaka F, Charkree K, Charoenchai L. The study of anti-inflammatory and antioxidant activity in cold press rice bran oil from rice in Thailand. Int J Pharm Pharm Sci 2014;6:428-31.8. Sukrasno S, Tuty S, Fidrianny I. Antioxidant evaluation and phytochemical content of various rice bran extracts of three varieties rice from Semarang, central Java, Indonesia. Asian J Pharm Clin Res 2017;10:377-82.9. Sabir A, Rafi M, Darusman LK. Discrimination of red and white rice bran from indonesia using HPLC fingerprint analysis combined with chemometrics. Food Chem 2017;221:1717-22.10. Niu Y, Gao B, Slavin M, Zhang X, Yang F, Bao J, et al. Phytochemical compositions, and antioxidant and anti-inflammatory properties of twenty-two red rice samples grown in Zhejiang. LWT Food Sci Technol 2013;54:521-7.11. Boonloh K, Kukongviriyapan V, Kongyingyoes B, Kukongviriyapan U, Thawornchinsombut S, Pannangpetch P, et al. Rice bran protein hydrolysates improve insulin resistance and decrease pro-inflammatory cytokine gene expression in rats fed a high carbohydrate-high fat diet. Nutrients 2015;7:6313-29.12. Peñarrieta JM, Alvarado JA, Akesson B, Bergenståhl B. Total antioxidant capacity and content of flavonoids and other phenolic compounds in canihua (Chenopodium pallidicaule): An andean pseudocereal. Mol Nutr Food Res 2008;52:708-17.13. Mungkhunthod S, Senggunprai L, Tangsucharit P, Sripui J, Kukongviriyapan U, Pannangpetch P. Antidesma thwaitesianum pomace extract improves insulin sensitivity via upregulation of PPAR-γ in high fat diet/streptozotocin-induced Type 2 diabetic rats. Asia Pac J Sci Technol 2016;21:63-76.14. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC, et al. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412-9.15. Naowaboot J, Wannasiri S. Anti-lipogenic effect of Senna alata leaf extract in high-fat diet-induced obese mice. Asian Pac J Trop Biomed 2016;6:232-8.16. Couturier K, Qin B, Batandier C, Awada M, Hininger-Favier I, Canini F, et al. Cinnamon increases liver glycogen in an animal model of insulin

ETHANOLIC EXTRACT OF TUBTIM-CHUMPHAE RICE BRAN DECREASES INSULIN RESISTANCE AND INTRAHEPATIC FAT ACCUMULATION IN HIGH-FAT-HIGH-FRUCTOSE DIET FED RATS

Objective: Tubtim-chumphae rice is hybrid Thai rice with a red pericarp. This study was aimed to investigate the effect of Tubtim-chumphae rice bran on insulin resistance and intrahepatic fat accumulation in high-fat-high-fructose diet (HFFD) fed rats.Methods: Ethanolic extract of rice bran (ERB) was prepared using a 50% ethanol-water. Male Sprague-Dawley rats were fed HFFD (40% lard, 20% fructose) for 10 weeks, followed by concomitant administrations of distilled water or ERB at 250 or 500 mg/kg/day or pioglitazone at 10 mg/kg/day for a further 4 weeks in treated groups. Normal control rats were fed normal chow and distilled water. At the end of all treatments, fasting blood glucose (FBG), an oral glucose tolerance test (OGTT), serum insulin levels, lipid profiles, and liver fat contents were measured. Liver histological and peroxisome proliferator-activated receptor-α (PPAR-α) gene expression examinations were performed.Results: At week 14, control HFFD rats had significantly (p&lt;0.05) higher FBG, low-density lipoprotein cholesterol, triglycerides, and insulin secretions together with impaired OGTT as compared to normal control rats. These parameters indicated an insulin resistant and dyslipidemic condition in HFFD rats. ERB 250 and 500 mg/kg or pioglitazone 10 mg/kg significantly ameliorated all of these changes. HFFD also caused a significant increase in fat accumulation and a decrease in PPAR-α gene expression in the livers which were significantly decreased by ERB.Conclusions: ERB decreases insulin resistance and intrahepatic fat accumulation possibly through increasing PPAR-α gene expression in HFFD rats. ERB might possibly be a neutraceutical for the metabolic syndrome patients.1. Gauthier MS, Favier R, Lavoie JM. Time course of the development of non-alcoholic hepatic steatosis in response to high-fat diet-induced obesity in rats. Br J Nutr 2006;95:273-81.2. Roberts CK, Hevener AL, Barnard RJ. Metabolic syndrome and insulin resistance: Underlying causes and modification by exercise training. Compr Physiol 2013;3:1-58.3. Grundy SM. Metabolic syndrome update. Trends Cardiovasc Med 2016;26:364-73.4. Fouret G, Gaillet S, Lecomte J, Bonafos B, Djohan F, Barea B, et al. 20-week follow-up of hepatic steatosis installation and liver mitochondrial structure and activity and their interrelation in rats fed a high-fat-high-fructose diet. Br J Nutr 2018;119:368-80.5. Dekker MJ, Su Q, Baker C, Rutledge AC, Adeli K. Fructose: A highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome. Am J Physiol Endocrinol Metab 2010;299:E685-94.6. Vichit W, Saewan N. Antioxidant activities and cytotoxicity of thai pigmented rice. Int J Pharm Pharm Sci 2015;7:329-34.7. Settharaksa S, Madaka F, Charkree K, Charoenchai L. The study of anti-inflammatory and antioxidant activity in cold press rice bran oil from rice in Thailand. Int J Pharm Pharm Sci 2014;6:428-31.8. Sukrasno S, Tuty S, Fidrianny I. Antioxidant evaluation and phytochemical content of various rice bran extracts of three varieties rice from Semarang, central Java, Indonesia. Asian J Pharm Clin Res 2017;10:377-82.9. Sabir A, Rafi M, Darusman LK. Discrimination of red and white rice bran from indonesia using HPLC fingerprint analysis combined with chemometrics. Food Chem 2017;221:1717-22.10. Niu Y, Gao B, Slavin M, Zhang X, Yang F, Bao J, et al. Phytochemical compositions, and antioxidant and anti-inflammatory properties of twenty-two red rice samples grown in Zhejiang. LWT Food Sci Technol 2013;54:521-7.11. Boonloh K, Kukongviriyapan V, Kongyingyoes B, Kukongviriyapan U, Thawornchinsombut S, Pannangpetch P, et al. Rice bran protein hydrolysates improve insulin resistance and decrease pro-inflammatory cytokine gene expression in rats fed a high carbohydrate-high fat diet. Nutrients 2015;7:6313-29.12. Peñarrieta JM, Alvarado JA, Akesson B, Bergenståhl B. Total antioxidant capacity and content of flavonoids and other phenolic compounds in canihua (Chenopodium pallidicaule): An andean pseudocereal. Mol Nutr Food Res 2008;52:708-17.13. Mungkhunthod S, Senggunprai L, Tangsucharit P, Sripui J, Kukongviriyapan U, Pannangpetch P. Antidesma thwaitesianum pomace extract improves insulin sensitivity via upregulation of PPAR-γ in high fat diet/streptozotocin-induced Type 2 diabetic rats. Asia Pac J Sci Technol 2016;21:63-76.14. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC, et al. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412-9.15. Naowaboot J, Wannasiri S. Anti-lipogenic effect of Senna alata leaf extract in high-fat diet-induced obese mice. Asian Pac J Trop Biomed 2016;6:232-8.16. Couturier K, Qin B, Batandier C, Awada M, Hininger-Favier I, Canini F, et al. Cinnamon increases liver glycogen in an animal model of insulin

Corrigendum.

CorrigendumCORRIGENDUMPublished Online:08 Oct 2018https://doi.org/10.1152/ajpendo.zh1-7977-corr.2018Original articleMoreSectionsPDF (84 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Pages E433–E447: Liu CW, Tsai HC, Huang CC, Tsai CY, Su YB, Lin MW, Lee KC, Hsieh YC, Li TH, Huang SF, Yang YY, Hou MC, Lin HC, Lee FY, Lee SD. Effects and mechanisms of caffeine to improve immunological and metabolic abnormalities in diet-induced obese rats. Am J Physiol Endocrinol Metab 314: E433–E447, 2018. First published November 7, 2017; doi:10.1152/ajpendo.00094.2017.—Author footnote symbol asterisk (*) was errantly inserted after the names of coauthors C.-W. Liu and H.-C. Lin, and the corresponding statement of co-first authorship between these authors was in error and should not have been included. The corrected author line appears as follows:Chih-Wei Liu,1,7 Hung-Cheng Tsai,4,7 Chia-Chang Huang,4,6,7 Chang-Youh Tsai,1,7 Yen-Bo Su,4,7 Ming-Wei Lin,5,7 Kuei-Chuan Lee,2,7 Yun-Cheng Hsieh,2,7 Tzu-Hao Li,4,7,8 Shiang-Fen Huang,3,7 Ying-Ying Yang,2,4,6,7 Ming-Chih Hou,2,7 Han-Chieh Lin,2,7 Fa-Yauh Lee,2,7 and Shou-Dong Lee7,9This article has no references to display. Download PDF Previous Back to Top FiguresReferencesRelatedInformation Related ArticlesEffects and mechanisms of caffeine to improve immunological and metabolic abnormalities in diet-induced obese rats 08 May 2018American Journal of Physiology-Endocrinology and Metabolism More from this issue > Volume 315Issue 4October 2018Pages E734-E734 Copyright & PermissionsCopyright © 2018 the American Physiological Societyhttps://doi.org/10.1152/ajpendo.zh1-7977-corr.2018PubMed30444639History Published online 8 October 2018 Published in print 1 October 2018 Metrics