scholarly journals Per-Arnt-Sim Kinase (PASK) Deficiency Increases Cellular Respiration on a Standard Diet and Decreases Liver Triglyceride Accumulation on a Western High-Fat High-Sugar Diet

Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1990 ◽  
Author(s):  
Jenny Pape ◽  
Colleen Newey ◽  
Haley Burrell ◽  
Audrey Workman ◽  
Katelyn Perry ◽  
...  
Keyword(s):  
The United States ◽  
Cellular Respiration ◽  
Standard Diet ◽  
Male Mice ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
High Sugar ◽  
Triglyceride Accumulation ◽  
Pas Kinase

Diabetes and the related disease metabolic syndrome are epidemic in the United States, in part due to a shift in diet and decrease in physical exercise. PAS kinase is a sensory protein kinase associated with many of the phenotypes of these diseases, including hepatic triglyceride accumulation and metabolic dysregulation in male mice placed on a high-fat diet. Herein we provide the first characterization of the effects of western diet (high-fat high-sugar, HFHS) on Per-Arnt-Sim kinase mice (PASK−/−) and the first characterization of both male and female PASK−/− mice. Soleus muscle from the PASK−/− male mice displayed a 2-fold higher oxidative phosphorylation capacity than wild type (WT) on the normal chow diet. PASK−/− male mice were also resistant to hepatic triglyceride accumulation on the HFHS diet, displaying a 2.7-fold reduction in hepatic triglycerides compared to WT mice on the HFHS diet. These effects on male hepatic triglyceride were further explored through mass spectrometry-based lipidomics. The absence of PAS kinase was found to affect many of the 44 triglycerides analyzed, preventing hepatic triglyceride accumulation in response to the HFHS diet. In contrast, the female mice showed resistance to hepatic triglyceride accumulation on the HFHS diet regardless of genotype, suggesting the effects of PAS kinase may be masked.

scholarly journals Gut Microbiota Regulates the Interplay between Diet and Genetics to Influence Glucose Tolerance †

Proceedings ◽  
2020 ◽  
Vol 61 (1) ◽  
pp. 17
Author(s):  
Jeralyn J. Franson ◽  
Julianne H. Grose ◽  
Kaitlyn Williams Larson ◽  
Laura C. Bridgewater
Keyword(s):  
Weight Gain ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Nutrient Sensing ◽  
Metabolic Effects ◽  
Leaky Gut ◽  
Liver Triglyceride ◽  
High Fat ◽  
Triglyceride Accumulation ◽  
Pas Kinase

Per-arnt-sim (PAS) kinase is a nutrient sensing serine/threonine kinase whose absence protects against triglyceride accumulation, insulin resistance, a decreased metabolic rate and increased weight gain in response to a high fat diet, using phenotypes associated with the gut microbiome. Herein we further explored the metabolic effects of PAS kinase-deficiency(PASK−/−) on a high fat high sugar (HFHS) diet, including contributions from an altered microbiome. PASK−/− mice were not protected from weight gain on the HFHS diet but were resistant to liver triglyceride accumulation. Microbiome analysis of both WT and PASK−/− mice revealed a forked shift with two discrete clusters of HFHS-fed mice emerging, which displayed increased beta and decreased alpha diversity compared with the normal chow diet (NCD). A “lower” cluster associated with both increased weight gain and glucose intolerance contained elevated levels of Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria and Defferibacteres. Lower cluster PASK−/− mice also influenced glucose tolerance and Claudin-1 expression, a protein associated with leaky gut. These results suggest PAS kinase-deficiency can protect mice against the deleterious effects of liver triglyceride accumulation, leaky gut and glucose intolerance in response to diet; however, microbiome imbalance can override protection. In addition, these results support a healthy diet and suggest microbial culprits associated with metabolic disease.

scholarly journals Gut Microbiota Regulates the Interaction between Diet and Genetics to Influence Glucose Tolerance

Medicines ◽  
2021 ◽  
Vol 8 (7) ◽  
pp. 34
Author(s):  
Jeralyn Franson ◽  
Julianne Grose ◽  
Kaitlyn Larson ◽  
Laura Bridgewater
Keyword(s):  
Weight Gain ◽  
Gut Microbiome ◽  
Alpha Diversity ◽  
Nutrient Sensing ◽  
Metabolic Effects ◽  
High Fat ◽  
Serine Threonine Kinase ◽  
16S Sequencing ◽  
Triglyceride Accumulation ◽  
Pas Kinase

Background: Metabolic phenotypes are the result of an intricate interplay between multiple factors, including diet, genotype, and the gut microbiome. Per–Arnt–Sim (PAS) kinase is a nutrient-sensing serine/threonine kinase, whose absence (PASK−/−) protects against triglyceride accumulation, insulin resistance, and weight gain on a high-fat diet; conditions that are associated with dysbiosis of the gut microbiome. Methods: Herein, we report the metabolic effects of the interplay of diet (high fat high sugar, HFHS), genotype (PASK−/−), and microbiome (16S sequencing). Results: Microbiome analysis identified a diet-induced, genotype-independent forked shift, with two discrete clusters of HFHS mice having increased beta and decreased alpha diversity. A “lower” cluster contained elevated levels of Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria and Defferibacteres, and was associated with increased weight gain, glucose intolerance, triglyceride accumulation, and decreased claudin-1 expression. Genotypic effects were observed within the clusters, lower cluster PASK−/− mice displayed increased weight gain and decreased triglyceride accumulation, whereas upper PASK−/− were resistant to decreased claudin-1. Conclusions: These results confirm previous reports that PAS kinase deficiency can protect mice against the deleterious effects of diet, and they suggest that microbiome imbalances can override protection. In addition, these results support a healthy diet for beneficial microbiome maintenance and suggest microbial culprits associated with metabolic disease.

scholarly journals Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Vanessa Caruline Araujo-Silva ◽  
Alice Santos-Silva ◽  
Andressa Silva Lourenço ◽  
Cristielly Maria Barros-Barbosa ◽  
Rafaianne Queiroz Moraes-Souza ◽  
...  
Keyword(s):  
Maternal Diabetes ◽  
Diabetic Rats ◽  
Female Rats ◽  
Gravid Uterus ◽  
Oral Glucose ◽  
Standard Diet ◽  
High Fat ◽  
High Sugar ◽  
Obesity And Diabetes

Embryo-fetal exposure to maternal disorders during intrauterine life programs long-term consequences for the health and illness of offspring. In this study, we evaluated whether mild diabetic rats that were given high-fat/high-sugar (HF/HS) diet presented maternal and fetal changes at term pregnancy. Female rats received citrate buffer (non-diabetic-ND) or streptozotocin (diabetic-D) after birth. According to the oral glucose tolerance test (OGTT), the experimental groups (n = 11 animals/group) were composed of non-diabetic and diabetic receiving standard diet (S) or HF/HS diet. High-fat/high-sugar diet (30% kcal of lard) in chow and water containing 5% sucrose and given 1 month before mating and during pregnancy. During and at the end of pregnancy, obesity and diabetes features were determined. After laparotomy, blood samples, periovarian fat, and uterine content were collected. The diabetic rats presented a higher glycemia and percentage of embryonic losses when compared with the NDS group. Rats DHF/HS presented increased obesogenic index, caloric intake, and periovarian fat weight and reduced gravid uterus weight in relation to the other groups. Besides, this association might lead to the inflammatory process, confirmed by leukocytosis. Obese rats (NDHF/HS and DHF/HS) showed higher triglyceride levels and their offspring with lower fetal weight and ossification sites, indicating intrauterine growth restriction. This finding may contribute to vascular alterations related to long-term hypertensive disorders in adult offspring. The fetuses from diabetic dams showed higher percentages of skeletal abnormalities, and DHF/HS dams still had a higher rate of anomalous fetuses. Thus, maternal diabetes and/or obesity induces maternal metabolic disorders that contribute to affect fetal development and growth.

Beet (Beta vulgaris L.) Stalk and Leaf Supplementation Improves Glucose Homeostasis and Insulin Resistance Markers in Liver of Mice Exposed to a High-Fat Diet

2020 ◽  
Author(s):  
Isabela Micheletti Lorizola ◽  
Josiane Érica Miyamoto ◽  
Ana Luiza Figueiredo Vieira ◽  
Beatriz Rocchetti Sumere ◽  
Rosângela Maria Neves Bezerra ◽  
...  
Keyword(s):  
Beta Vulgaris ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Standard Diet ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Treatment Groups ◽  
Triglyceride Content ◽  
Resistance Markers ◽  
Unhealthy Diet

Abstract Background Although beet stalks and leaves are not consumed and are usually discarded, they are an important source of bioactive flavonoids possessing antioxidant and anti-inflammatory activity, which could be explored to prevent metabolic disorders associated with an unhealthy diet. The aim of this study was to assess the effect of supplementation with beet (Beta vulgaris L.) stalks and leaves on metabolic parameters and glucose homeostasis in mice exposed to a high-fat diet.Methods Six-week-old male Swiss mice were randomly divided into five experimental groups submitted to either standard diet (CT) or high-fat diet (HF), and HF-fed mice were subdivided into three treatment groups supplemented with oven-dehydrated beet stalks and leaves (SL), lyophilized beet stalks and leaves (Ly) or beet stalk and leaf extract (EX).Results Supplementation with SL was able to ameliorate glucose homeostasis (P < 0.05) with no alteration in hepatic triglyceride content. It remains to be clarified if the enhancement in the glucose homeostasis observed in HFSL could be a consequence of improvement in pancreatic insulin secretion and/or glucose uptake from skeletal muscle and white adipose tissues.Conclusions The current results suggest that beet stalks and leaves could be used as adjuvants to improve parameters related to glucose metabolism in the liver.

Lepidium Meyenii Supplemented Diet Modulates Neurobehavioral and Biochemical Parameters in Mice Fed High-Fat-High-Sugar Diet

2020 ◽  
Vol 20 ◽  
Author(s):  
Anthony T. Olofinnade ◽  
Abiola Alawode ◽  
Adejoke Y. Onaolapo ◽  
Olakunle J. Onaolapo
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Body Weight ◽  
Inflammatory Markers ◽  
Acetylcholinesterase Activity ◽  
Standard Diet ◽  
High Fat ◽  
Lepidium Meyenii ◽  
High Sugar ◽  
Increased Risk

Background: Metabolic syndrome has been associated with increased risk of cardiovascular disease, diabetes mellitus, and neurodegenerative disorders. Known side-effects of currently-available drugs necessitate the search for possibly better treatment options. Objective: This study examined the effects of dietary lepidium meyenii (MACA) supplementation on neurobehaviour, metabolic profile, levels of inflammatory markers, and oxidative stress parameters in a mouse model of metabolic syndrome. Methodology: Mice were randomly-assigned into 8 groups of ten animals each. Groups consist of standard diet (SD) control, high fat/high sugar (HFHS) control and three groups each of lepidium meyenii incorporated into either SD or HFHS diet at 0.1, 0.2 and 0.4 %. Mice were fed for seven weeks, and body weight was measured weekly. Open-field behaviors and radial-arm/Y-maze spatial memory were scored at the end of the study. Twenty-four hours after the last behavioral test, fasting blood glucose levels were estimated. Animals were then euthanized, and blood taken for estimation of serum lipid profile. Whole brains were excised, weighed and homogenized for the estimation of levels of lipid peroxidation, inflammatory markers, antioxidant status, and acetylcholinesterase activity. Results: MACA-supplemented diet was associated with a decrease in body weight gain, an increase in food intake (at lower concentrations), suppression of grooming behavior, and decrease in acetylcholinesterase activity. MACA-supplement also reversed HFHS-induced memory impairment, anxiety, hyperglycaemia, lipid derangement, oxidative stress, and derangement of inflammatory markers. Conclusion: Dietary supplementation with MACA shows beneficial effects in mitigating the effects of metabolic syndrome on the brain in mice.

scholarly journals Comparative Effects of Native and Defatted Flaxseeds on Intestinal Enzyme Activity and Lipid Metabolism in Rats Fed a High-Fat Diet Containing Cholic Acid

Nutrients ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 1181 ◽  
Author(s):  
Paulina Opyd ◽  
Adam Jurgoński ◽  
Jerzy Juśkiewicz ◽  
Bartosz Fotschki ◽  
Jarosław Koza
Keyword(s):  
Lipid Metabolism ◽  
Cholic Acid ◽  
Lipid Absorption ◽  
Cholesterol Concentration ◽  
Control Group ◽  
Standard Diet ◽  
High Fat ◽  
Hepatic Expression ◽  
Beneficial Effects ◽  
Triglyceride Accumulation

We hypothesize that defatting is an important factor that can determine the beneficial effects of flaxseeds on rats with diet-induced disorders. The experiment lasts 8 weeks and is conducted on Wistar rats allocated to four groups as follows: a control group fed with a standard diet; a high-fat (HF) group fed with a diet containing 21% fat and 0.1% cholic acid as a stimulator of lipid absorption; an HF group fed a diet supplemented with 1% native flaxseeds; and an HF group fed a diet supplemented with 1% defatted flaxseeds. In the HF group, several unfavourable changes in the gut and lipid metabolism are observed. Supplementation of the HF diet with native flaxseeds prevent an increase in colonic β-glucuronidase activity, whereas dietary defatted flaxseeds increase mucosal disaccharidase activities in the small intestine (sucrose, maltase and lactase). Regardless of the form of supplementation, dietary flaxseeds increase bacterial glycolytic activity in the distal intestine and decrease hepatic fat, especially triglyceride, accumulation. Both flaxseed forms decrease lipid peroxidation in the kidneys and increase the blood HDL cholesterol concentration with the native form being more efficient in the former and the defatted form being more efficient in the latter. The lipid-modulating effects of defatted flaxseeds are associated with reduced hepatic expression of peroxisome proliferator-activated receptor α, which is not the case in terms of native flaxseeds. Dietary supplementation with a relatively small amount of flaxseeds can exert beneficial effects on gut functions and lipid metabolism in rats, and these effects are affected by defatting to some extent.

scholarly journals The effects of chronic AMPK activation on hepatic triglyceride accumulation and glycerol 3-phosphate acyltransferase activity with high fat feeding

2013 ◽  
Vol 5 (1) ◽  
pp. 29 ◽  
Author(s):  
Bradley S Henriksen ◽  
Mary E Curtis ◽  
Natasha Fillmore ◽  
Brandon R Cardon ◽  
David M Thomson ◽  
...  
Keyword(s):  
Ampk Activation ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Acyltransferase Activity ◽  
Triglyceride Accumulation ◽  
Fat Feeding

scholarly journals Different Doses of Curcumin Supplementation Did Not Improve Biochemical Profile and Weight in C57BL/6 Male Mice Receiving High-Fat Diet

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 699-699
Author(s):  
Caroline Silva ◽  
Priscila Fassini ◽  
Leandra Ramalho ◽  
Daniela Sartori ◽  
Vivian Suen
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Statistical Significance ◽  
Control Diet ◽  
Standard Diet ◽  
Biochemical Profile ◽  
Male Mice ◽  
High Fat ◽  
Pancreatic Steatosis ◽  
Different Doses

Abstract Objectives Curcuma supplementation has been investigated to prevent or treat obesity. However, evidence suggests development of pancreatic steatosis as well. In this context, the aim of this study was to investigate the effect of different doses of curcumin supplementation on weight, biochemical profile, and histological analysis of the pancreas and liver of mice fed a high-fat diet. Methods This was an experimental, longitudinal and randomized study. Fifty C57BL/6 male mice, thirty days age, were separated into five groups: 1. Standard diet (n = 10); 2. High-fat diet (n = 10); 3. High-fat diet plus 50 mg of curcumin/kg of body weight (n = 10); 4. High-fat diet plus 250 mg of curcumin/kg of body weight (n = 10); 5. High-fat diet plus 500 mg of curcumin/kg of body weight (n = 10). Group 1 was fed a standard control diet (AIN 93 G), group 2 was fed a purified high-fat diet (AIN 93 HF 60%) and both groups received only the vehicle (carboxymethyl cellulose - CMC 1%) by gavage. Mice from groups 3, 4 and 5 were fed a purified high-fat diet (AIN 93 HF 60%) plus curcumin at different doses (50, 250 and 500 mg/kg of body weight diluted in 1% CMC) by gavage for twelve weeks. All groups received food and water ad libitum. At the end of the experimental period, we analysed lipid profile, blood glucose, insulin, histology of the pancreas and liver. ANOVA one way and Kruskal-Wallis analysis were performed and a value of P ˂ 0.05 was used to denote statistical significance. Results Curcumin supplementation did not improve weight and biochemical profile. Additionally, histological changes were not observed at any dose of supplementation. Pancreatic or hepatic steatosis was not evidenced in high-fat diet groups and also in the groups who received curcumin, suggesting no toxic effects at the different doses of supplementation provided. Conclusions Our results suggest that curcumin supplementation has no beneficial effect on weight gain prevention and biochemical profile, regardless of the dose administered. Funding Sources FAPESP (São Paulo Research Foundation).

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