Dietary Fat, but Not Protein or Carbohydrate, Regulates Energy Intake and Causes Adiposity in Mice

Hu, Sumei; Wang, Lu; Yang, Dengbao; Li, Li; Togo, Jacques; Wu, Ye; Liu, Quansheng; Li, Baoguo; Li, Min; Wang, Guanlin; Zhang, Xueying; Niu, Chaoqun; Li, Jianbo; Xu, Ye; Couper, Elspeth; Whittington-Davies, Andrew; Mazidi, Mohsen; Luo, Lijuan; Wang, Shengnan; Douglas, Alex; Speakman, John R.

doi:10.1016/j.cmet.2018.06.010

Cited by 215 publications

(223 citation statements)

References 59 publications

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“…29 At the same time, caloric intake was higher in the HFD versus the SD group (Figure 4) and this result 30 is in accordance with the literature (Hu et al, 2018a;Kleinert et al, 2018;Yang et al, 2014). The 31 high energy density found in the HFD (5.439 kcal/g) compared to the SD (3.080 kcal/g), particularly 32 from fat (58.2% vs 11.7%, respectively), support the caloric intake higher in the HFD group and it is 33 in accordance to a recent study where the authors suggested that the amount of fat from an HFD, but 34 not protein or carbohydrate, is the cause of adiposity increases in mice (Hu et al, 2018a). Further, we 35 also found an increase of adipose tissue in the HFD groups when compared to SD groups for 1 retroperitoneal (Figure 5 A) and epididymal adipose tissue (Figure 5 B).…”

Section: Differential Gene Expression In the Nucleus Accumbens -Transsupporting

confidence: 82%

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

Brandão¹,

Bonet

Pagliusi³

et al. 2019

Preprint

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4High-fat diet (HFD)-induced obesity was reported to increase pain behavior independent of obesity 5 status in rats, whereas weight loss interventions such as voluntary physical activity (PA) for adults 6 with overweight or obesity was reported to promote pain reduction in humans with chronic pain (CP). 7 However, is unknown whether an HFD and sedentary (SED) behavior is underlying to CP 8 susceptibility and whether voluntary PA can prevent it. Moreover, differential gene expression in the 9 nucleus accumbens (NAc) is considered to play a crucial role in CP susceptibility. The present study 10 used an adapted model of the inflammatory prostaglandin E2 (PGE)-induced persistent hyperalgesia 11 (PH-ST) protocol for mice, an HFD, and a voluntary PA paradigm to test these hypotheses. In 12 addition, we performed a transcriptome in the NAc and a gene ontology enrichment tools to 13 investigate the differential gene expression and identify the biological processes associated with CP 14 susceptibility tested here. Our results demonstrated that HFD and sedentary behavior promoted CP 15 susceptibility, which in turn was prevented by voluntary PA, even when the animals were fed an 16 HFD. Transcriptome in the NAc found 2,204 differential expression genes related CP susceptibility 17 promoted by HFD and sedentary behavior and prevented by voluntary PA. The gene ontology 18 enrichment revealed 41 biological processes implicated in CP susceptibility. Analyzing collectively 19 those biological processes, our results suggested that genes related to metabolic and mitochondria 20 stress were up-regulated in the CP susceptibility group, whereas genes related to neuroplasticity and 21 axonogenesis were up-regulated in the CP prevented group. These findings provide pieces of 22 evidence that an HFD and sedentary behavior promoted gene expression changes in the NAc related 23 to neurodegeneration and those changes were also underlying to CP susceptibility. Additionally, our 24 findings confirmed other findings supporting the crucial role of voluntary PA to prevent CP 25 susceptibility and add novel insights of differential gene expression in the NAc related to 26 neuroplasticity. 27 28

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Section: Differential Gene Expression In the Nucleus Accumbens -Transsupporting

confidence: 82%

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

Brandão¹,

Bonet

Pagliusi³

et al. 2019

Preprint

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show abstract

“…High‐fat diet is a widely adopted method to induce obesity, non‐alcoholic fatty liver and T2DM, in which IR is widely considered the ‘common soil’ of those metabolic disorders . Maternal obesity is afflicted with many maternal obstetric complications in the offspring including high blood pressure, obesity, gestational diabetes and increased perinatal morbidity .…”

Section: Discussionmentioning

confidence: 99%

“…Our data confirmed that HFD led to IR and metabolic High-fat diet is a widely adopted method to induce obesity, non-alcoholic fatty liver and T2DM, in which IR is widely considered the 'common soil' of those metabolic disorders. [20][21][22] Maternal obesity is afflicted with many maternal obstetric complications in the offspring including high blood pressure, obesity, gestational diabetes and increased perinatal morbidity. 23 Several factors are involved in the progression of IR induced by HFD including inflammation, excessive ROS, abnormal immune response, lipotoxicity and altered glycosylation.…”

Section: Discussionmentioning

confidence: 99%

P53/PANK1/miR‐107 signalling pathway spans the gap between metabolic reprogramming and insulin resistance induced by high‐fat diet

Yang

Zhang

Wang

et al. 2020

J Cellular Molecular Medi

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High‐fat diet (HFD) leads to obesity, type II diabetes mellitus (T2DM) and increases the coincidence of cardiovascular diseases and cancer. Insulin resistance (IR) is considered as the ‘common soil’ of those diseases. Furthermore, people on HFD showed restrained glycolysis and enhanced fatty acid oxidation, which is the so‐called metabolic reprogramming. However, the relationship between metabolic reprogramming and IR induced by HFD is still unclear. Here, we demonstrate that PANK1 and miR‐107 were up‐regulated in the liver tissue of mice on HFD for 16 weeks and involved in metabolic reprogramming induced by palmitate acid (PA) incubation. Importantly, miR‐107 within an intron of PANK1 gene facilitated IR by targeting caveolin‐1 in AML12 cells upon PA incubation. Moreover, we identify that HFD enhanced P53 expression, and activation of P53 with nutlin‐3a induced PANK1 and miR‐107 expression simultaneously in transcriptional level, leading to metabolic reprogramming and IR, respectively. Consistently, inhibition of P53 with pifithrin‐α hydrobromide ameliorated PA‐induced metabolic reprogramming and IR. Thus, our results revealing a new mechanism by which P53 regulate metabolism. In addition, the results distinguished the different roles of PANK1 and its intron miR‐107 in metabolic regulation, which will provide more accurate intervention targets for the treatment of metabolic diseases.

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“…However, it has been reported to cause acute pancreatitis and kidney failure in some patients (Hu et al, 2018). However, it has been reported to cause acute pancreatitis and kidney failure in some patients (Hu et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…One of the most recent therapies for T2D, Byetta, targets GLP-1 receptors on β-cells to stimulate insulin secretion, and studies in mice suggest that it also increases β-cell mass. However, it has been reported to cause acute pancreatitis and kidney failure in some patients (Hu et al, 2018). Therefore, there is a need for the development of novel therapies with minimal side effects that can enhance pancreatic β-cell function and β-cell mass for glucose utilization.…”

Section: Introductionmentioning

confidence: 99%

Quercetin modulates hyperglycemia by improving the pancreatic antioxidant status and enzymes activities linked with glucose metabolism in type 2 diabetes model of rats: In silico studies of molecular interaction of quercetin with hexokinase and catalase

et al. 2019

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Quercetin was assessed for its antihyperglycemic effect in fructose-streptozotocin (STZ) induced diabetic rats. The oral administration of quercetin at the dosage of 25 and 50 mg/kg for 28 days remarkably reduced the level of blood glucose, glycosylated hemoglobin (Hb), and hepatic glycogen but enhanced plasma Hb concentration. The altered activities of glucose-6-phosphatase and hexokinase in diabetic rats were significantly improved upon quercetin treatment. Furthermore, the antioxidant activity of pancreatic superoxide dismutase, catalase (CAT), and reduced glutathione was effectively increased while the value for thiobarbituric acid reactive species was decreased. A significant reduction of glycemia was observed in the glucose tolerance test, 120 min after the glucose pulse. Also, the damage caused by fructose-STZ in the liver and pancreas of diabetic animals were restored to near normal. Molecular docking of quercetin showed a high affinity for hexokinase and CAT with a binding energy of −7.82 and −9.83 kcal/mol, respectively, more elevated than the standard drugs. Practical applicationsFunctional foods and nutraceuticals have increasingly interested the consumers in terms of health benefits and have started focussing on the prevention or cure of disease by the foods and their health-enhancing phytochemicals. Quercetin is one of the most potent naturally occurring antioxidants within the flavonoid subclasses, mostly distributed as a secondary metabolite in fruits, vegetables, and black tea.Based on the results exhibited in the present study, we proposed that the consumption of foods rich in quercetin could be a cheap and affordable nutraceutical that can be developed for the treatment of T2DM and its complications. Further studies on the safety aspects of quercetin in long-term usage are strongly recommended before implementing for the treatment of human diseases. | MATERIAL S AND ME THODS | Chemicals and reagentsThe compounds 3,5,7,3,4, pentahydroxy flavones (quercetin), STZ, potassium hydroxide (KOH), cyanmethemoglobin, trichloroacetic acid (TCA), sulfuric acid (H 2 SO 4 ), HPLC grade ethanol, potassium chloride (KCl), ethylenediaminetetraacetic acid (EDTA), ammonium molybdate {(NH4) 6 Mo 7 O 24 }, ammonium acetate (NH 4 CH 3 CO 2 ), K E Y W O R D S anti-hyperglycaemic, antioxidant, glucose metabolism, histopathology, molecular docking, Quercetin | 3 of 16 OYEDEMI Et al.amino naphthol sulfonic acid (C 10 H 9 NO 4 S), Tris-HCl buffer, citrate buffer, sucrose, glucose, and Drabkin reagents purchased from Merck Chemicals (Pty) Ltd., Bellville, South Africa. All other chemicals and reagents were of analytical grade and procured from Sigma-Aldrich Chemical Co. (Johannesburg-SA).

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Dietary Fat, but Not Protein or Carbohydrate, Regulates Energy Intake and Causes Adiposity in Mice

Cited by 215 publications

References 59 publications

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

P53/PANK1/miR‐107 signalling pathway spans the gap between metabolic reprogramming and insulin resistance induced by high‐fat diet

Quercetin modulates hyperglycemia by improving the pancreatic antioxidant status and enzymes activities linked with glucose metabolism in type 2 diabetes model of rats: In silico studies of molecular interaction of quercetin with hexokinase and catalase

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