Acute Hyperenergetic, High-Fat Feeding Increases Circulating FGF21, LECT2, and Fetuin-A in Healthy Men

Willis, Scott A.; Sargeant, Jack A; Yates, Thomas; Takamura, Toshinari; Takayama, Hiroaki; Gupta, Vinay; Brittain, Emily; Crawford, Joe; Parry, Siôn A; Thackray, Alice E.; Varela-Mato, Verónica; Stensel, David J.; Woods, Rachel; Hulston, Carl J.; Aithal, Guruprasad P.; King, James A.

doi:10.1093/jn/nxz333

Cited by 29 publications

(28 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A limitation of this study is that we cannot provide mechanistic insight; however, it is possible that augmented circulating insulin was responsible for stimulating leptin production from adipocytes [39]. We have reported previously that fasted circulating insulin, and insulin responses to the OGTT, were elevated in response to the HE-HFD [30]. The physiological relevance of the leptin response to overfeeding is not clear.…”

Section: Discussionmentioning

confidence: 90%

“…This manuscript presents secondary endpoints from data collected in a study investigating hepatokine and metabolic responses to overfeeding; a detailed description of the study design and results of the primary study outcomes have been published [30]. After receiving institutional ethical approval, 12 healthy males were recruited into the study after providing written informed consent.…”

Section: Ethical Approval and Participant Recruitmentmentioning

confidence: 99%

“…At the baseline (pre-diet) and seven-day visits, participants additionally underwent a 2 h oral glucose tolerance test (OGTT). During this test, appetite ratings were assessed at 0 h (fasted), 1 h and 2 h after the consumption of 82.5 g of dextrose monohydrate (MyProtein, Cheshire, UK) and the mean response across 2 h was calculated for each rating (note: insulin and glucose data have been published previously [30]). Within each dietary intervention, participants were instructed not to alter their habitual physical activity levels and compliance with this request was confirmed via accelerometry (data published previously [30]).…”

Section: Study Design and Proceduresmentioning

confidence: 99%

“…The data reported in this manuscript are secondary outcomes from a previous trial [30], and consequently, the sample size was not informed by a formal power calculation.…”

Section: Statistical Analysesmentioning

confidence: 99%

“…HE-HFD, hyperenergetic high-fat diet; VAS, visual analogue scale; OGTT, oral glucose tolerance test; LFPQ, Leeds Food Preference Questionnaire. * Physical activity, sitting time and food intake data collected during the control diet and the HE-HFD have been reported previously[30].…”

mentioning

confidence: 99%

See 4 more Smart Citations

Influence of Short-Term Hyperenergetic, High-Fat Feeding on Appetite, Appetite-Related Hormones, and Food Reward in Healthy Men

et al. 2020

Self Cite

View full text Add to dashboard Cite

Short-term overfeeding may provoke compensatory appetite responses to correct the energy surplus. However, the initial time-course of appetite, appetite-related hormone, and reward-related responses to hyperenergetic, high-fat diets (HE-HFD) are poorly characterised. Twelve young healthy men consumed a HE-HFD (+50% energy, 65% fat) or control diet (36% fat) for seven days in a randomised crossover design. Mean appetite perceptions were determined during an oral glucose tolerance test (OGTT) before and after each diet. Fasted appetite perceptions, appetite-related hormones, and reward parameters were measured pre-diet and after 1-, 3- and 7-days of each diet. The HE-HFD induced a pre-to-post diet suppression in mean appetite during the OGTT (all ratings p ≤ 0.058, effect size (d) ≥ 0.31), and reduced the preference for high-fat vs. low-fat foods (main effect diet p = 0.036, d = 0.32). Fasted leptin was higher in the HE-HFD than control diet (main effect diet p < 0.001, d = 0.30), whilst a diet-by-time interaction (p = 0.036) revealed fasted acylated ghrelin was reduced after 1-, 3- and 7-days of the HE-HFD (all p ≤ 0.040, d ≥ 0.50 vs. pre-diet). Appetite perceptions and total peptide YY in the fasted state exhibited similar temporal patterns between the diets (diet-by-time interaction p ≥ 0.077). Seven days of high-fat overfeeding provokes modest compensatory changes in subjective, hormonal, and reward-related appetite parameters.

show abstract

Section: Discussionmentioning

confidence: 90%

Section: Ethical Approval and Participant Recruitmentmentioning

confidence: 99%

Section: Study Design and Proceduresmentioning

confidence: 99%

“…The data reported in this manuscript are secondary outcomes from a previous trial [30], and consequently, the sample size was not informed by a formal power calculation.…”

Section: Statistical Analysesmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Influence of Short-Term Hyperenergetic, High-Fat Feeding on Appetite, Appetite-Related Hormones, and Food Reward in Healthy Men

et al. 2020

Self Cite

View full text Add to dashboard Cite

show abstract

Contribution of organokines in the development of NAFLD/NASH associated hepatocellular carcinoma

Vachher

Bansal

Kumar

et al. 2022

J of Cellular Biochemistry

View full text Add to dashboard Cite

Globally the incidence of hepatocellular carcinoma (HCC) is on an upsurge. Evidence is accumulating that liver disorders like nonalcoholic fatty liver disease (NAFLD) and its more progressive form nonalcoholic steatohepatitis (NASH) are associated with increased risk of developing HCC. NAFLD has a prevalence of about 25% and 50%–90% in obese population. With the growing burden of obesity epidemic worldwide, HCC presents a major healthcare burden. While cirrhosis is one of the major risk factors of HCC, available literature suggests that NAFLD/NASH associated HCC also develops in minimum or noncirrhotic livers. Therefore, there is an urgent need to understand the pathogenesis and risk factors associated with NAFLD and NASH related HCC that would help in early diagnosis and favorable prognosis of HCC secondary to NAFLD. Adipokines, hepatokines and myokines are factors secreted by adipocytes, hepatocytes and myocytes, respectively, playing essential roles in cellular homeostasis, energy balance and metabolism with autocrine, paracrine and endocrine effects. In this review, we endeavor to focus on the role of these organokines in the pathogenesis of NAFLD/NASH and its progression to HCC to augment the understanding of the factors stimulating hepatocytes to acquire a malignant phenotype. This shall aid in the development of novel therapeutic strategies and tools for early diagnosis of NAFLD/NASH and HCC.

show abstract

The molecular structure and role of LECT2 or CHM‐II in arthritis, cancer, and other diseases

Zhu

Bennett

et al. 2021

Journal Cellular Physiology

View full text Add to dashboard Cite

Leukocyte cell-derived chemotaxin-2 (LECT2 or LECT-2), also called chondromodulin II (ChM-II or CHM2) plays a versatile role in various tissues. It was first identified as a chemotactic factor to promote the migration of neutrophils. It was also reported as a hepatokine to regulate glucose metabolism, obesity, and nonalcoholic fatty liver disease. As a secreted factor, LECT2 binds to several cell surface receptors CD209a, Tie1, and Met to regulate inflammatory reaction, fibrogenesis, vascular invasion, and tumor metastasis in various cell types. As an intracellular molecule, it is associated with LECT2-mediated amyloidosis, in which LECT2 misfolding results in insoluble fibrils in multiple tissues such as the kidney, liver, and lung. Recently, LECT2 was found to be associated with the development of rheumatoid arthritis and osteoarthritis, involving the dysregulation of osteoclasts, mesenchymal stem cells, osteoblasts, chondrocytes, and endothelial cells in the bone microenvironment. LECT2 is implicated in the development of cancers, such as hepatocellular carcinoma via MET-mediated PTP1B/Raf1/ERK signaling pathways and is proposed as a biomarker. The mechanisms by which LECT2 regulates diverse pathogenic conditions in various tissues remain to be fully elucidated. Further research to understand the role of LECT2 in a tissue tropism-dependent manner would facilitate the development of LECT2 as a biomarker for diagnosis and therapeutic target.

show abstract

Acute Hyperenergetic, High-Fat Feeding Increases Circulating FGF21, LECT2, and Fetuin-A in Healthy Men

Cited by 29 publications

References 67 publications

Influence of Short-Term Hyperenergetic, High-Fat Feeding on Appetite, Appetite-Related Hormones, and Food Reward in Healthy Men

Influence of Short-Term Hyperenergetic, High-Fat Feeding on Appetite, Appetite-Related Hormones, and Food Reward in Healthy Men

Contribution of organokines in the development of NAFLD/NASH associated hepatocellular carcinoma

The molecular structure and role of LECT2 or CHM‐II in arthritis, cancer, and other diseases

Contact Info

Product

Resources

About