scholarly journals High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2140
Author(s):  
Yumiko Takahashi ◽  
Yutaka Matsunaga ◽  
Hiroki Yoshida ◽  
Terunaga Shinya ◽  
Ryo Sakaguchi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transporter ◽  
High Carbohydrate Diet ◽  
Oral Glucose ◽  
Carbohydrate Diet ◽  
Post Exercise ◽  
Glucose Administration ◽  
Protein Levels ◽  
High Carbohydrate ◽  
Glucose Transporter 2

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.

Effect of diet on glucose transporter site density along the intestinal crypt-villus axis

1992 ◽  
Vol 262 (6) ◽  
pp. G1060-G1068 ◽  
Author(s):  
R. P. Ferraris ◽  
S. A. Villenas ◽  
B. A. Hirayama ◽  
J. Diamond
Keyword(s):  
Brush Border ◽  
Glucose Transporter ◽  
Binding Constants ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Site Density ◽  
Phlorizin Binding ◽  
High Affinity Binding Site ◽  
A Site

High-carbohydrate diets stimulate intestinal brush-border glucose uptake and increase the number of glucose-protectable phlorizin binding sites, but it has been unknown where along the crypt-villus axis these effects are expressed. We attacked this problem by three methods. First, by measuring phlorizin binding to isolated mouse enterocytes fractionated along the crypt-villus axis by the Weiser method, we identified a high-affinity binding site predominating from villus tip to midvillus and a site of possibly lower affinity predominating in the crypts. A high-carbohydrate diet increased by severalfold the density of the villus sites and probably also of the crypt sites, without changing their binding constants. Second, autoradiography revealed increased glucose-protectable phlorizin binding along the whole crypt-villus axis on a high-carbohydrate diet. Finally, a polyclonal antibody against the Na(+)-glucose cotransporter recognized a protein in the brush-border membrane of villus cells. Hence, substrate-dependent upregulation of intestinal glucose transport involves increased numbers of transporters along the crypt-villus axis.

scholarly journals Effects of a high-fat, high-carbohydrate diet on blood cells of rats

2021 ◽  
Vol 20 (3) ◽  
pp. 6-12
Author(s):  
J. G. Birulina ◽  
V. V. Ivanov ◽  
E. E. Buyko ◽  
O. A. Trubacheva ◽  
I. V. Petrova ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
High Carbohydrate Diet ◽  
Control Group ◽  
Oral Glucose ◽  
High Fat ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Kca Channels ◽  
Induced Aggregation ◽  
Experimental Group

Aim. To study the effects of a high-fat, high-carbohydrate diet on erythrocytes and platelets of rats.Materials and methods. Male Wistar rats (n = 23) were used for the study. The rats were divided into a control group and an experimental group. The rats from the control group were fed with standard rat chow. The rats from the experimental group had received a high-fat and high-carbohydrate diet for 12 weeks. In the rats, body weight and blood pressure (BP) were measured, an oral glucose tolerance test was carried out, and hematological and lipid metabolism parameters were analyzed. The conductance of erythrocyte KCa-channels was measured by the potentiometric method, and platelet aggregation was determined by the turbidimetric method.Results. Feeding the rats with a high-fat, high-carbohydrate diet for 12 weeks resulted in obesity, BP elevation, hyperglycemia, impaired glucose tolerance, and dyslipidemia with pronounced triglyceridemia. In the experimental group, a rise in the number of leukocytes, mainly due to granulocytes, and an increase in the number of platelets and their collagen-induced aggregation were observed. The red blood cell count in the rats of the experimental group did not significantly differ from that of the control group. In the experimental group, multidirectional changes in the membrane potential were observed in response to the stimulation of the KCa-channels in the erythrocyte membrane with the Ca2+ ionophore A23187 or artificial redox systems.Conclusion. The obtained data indicate that a high-fat, high-carbohydrate diet leads to metabolic and hemorheological disorders that are typical of metabolic syndrome.

scholarly journals Genome wide analysis in Drosophila reveals diet by gene interactions and uncovers diet-responsive genes

2021 ◽  
Author(s):  
Deanne Francis ◽  
Shila Ghazanfar ◽  
Essi Havula ◽  
James R Krycer ◽  
Dario Strbenac ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Inbred Strains ◽  
High Carbohydrate Diet ◽  
Whole Body ◽  
Starvation Resistance ◽  
Nutrient Storage ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Important Health ◽  
Genetic And Environmental Factors

Abstract Genetic and environmental factors play a major role in metabolic health. However, they do not act in isolation, as a change in an environmental factor such as diet may exert different effects based on an individual’s genotype. Here, we sought to understand how such gene-diet interactions influenced nutrient storage and utilization, a major determinant of metabolic disease. We subjected 178 inbred strains from the Drosophila Genetic Reference Panel (DGRP), to diets varying in sugar, fat and protein. We assessed starvation resistance, a holistic phenotype of nutrient storage and utilization that can be robustly measured. Diet influenced the starvation resistance of most strains, but the effect varied markedly between strains such that some displayed better survival on a high carbohydrate diet compared to a high fat diet while others had opposing responses, illustrating a considerable gene x diet interaction. This demonstrates that genetics plays a major role in diet responses. Furthermore, heritability analysis revealed that the greatest genetic variability arose from diets either high in sugar or high in protein. To uncover the genetic variants that contribute to the heterogeneity in starvation resistance, we mapped 566 diet-responsive SNPs in 293 genes, 174 of which have human orthologues. Using whole-body knockdown, we identified two genes that were required for glucose tolerance, storage and utilization. Strikingly, flies in which the expression of one of these genes, CG4607 a putative homolog of a mammalian glucose transporter, was reduced at the whole-body level, displayed lethality on a high carbohydrate diet. This study provides evidence that there is a strong interplay between diet and genetics in governing survival in response to starvation, a surrogate measure of nutrient storage efficiency and obesity. It is likely that a similar principle applies to higher organisms thus supporting the case for nutrigenomics as an important health strategy.

scholarly journals A high-carbohydrate diet induces greater inflammation than a high-fat diet in mouse skeletal muscle

2020 ◽  
Vol 53 (3) ◽  
Author(s):  
M.M. Antunes ◽  
G. Godoy ◽  
C.B. de Almeida-Souza ◽  
B.A. da Rocha ◽  
L.G. da Silva-Santi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Fat Diet ◽  
High Carbohydrate Diet ◽  
High Fat ◽  
Carbohydrate Diet ◽  
Mouse Skeletal Muscle ◽  
High Carbohydrate

scholarly journals Improvement of Obesity and Dyslipidemic Activity of Amomum tsao-ko in C57BL/6 Mice Fed a High-Carbohydrate Diet

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1638
Author(s):  
Ju-Hyoung Park ◽  
Eun-Kyung Ahn ◽  
Min Hee Hwang ◽  
Young Jin Park ◽  
Young-Rak Cho ◽  
...  
Keyword(s):  
Body Weight Gain ◽  
Subcutaneous Fat ◽  
Density Lipoprotein ◽  
Ethanol Extract ◽  
Cardiac Risk ◽  
Normal Diet ◽  
High Carbohydrate Diet ◽  
Atherogenic Index ◽  
Carbohydrate Diet ◽  
High Carbohydrate

Amomum tsao-ko Crevost et Lemaire (Zingiberaceae) is a medicinal herb found in Southeast Asia that is used for the treatment of malaria, abdominal pain, dyspepsia, etc. The aim of this study was to investigate the effect of an ethanol extract of Amomum tsao-ko (EAT) on obesity and hyperlipidemia in C57BL/6 mice fed a high-carbohydrate diet (HCD). First, the mice were divided into five groups (n = 6/group) as follows: normal diet, HCD, and HCD+EAT (100, 200, and 400 mg/kg/day), which were orally administered with EAT daily for 84 days. Using microcomputed tomography (micro-CT) analysis, we found that EAT inhibited not only body-weight gain, but also visceral fat and subcutaneous fat accumulation. Histological analysis confirmed that EAT decreased the size of fat tissues. EAT consistently improved various indices, including plasma levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein, high-density lipoprotein, atherogenic index, and cardiac risk factors, which are related to dyslipidemia—a major risk factor for heart disease. The contents of TC and TG, as well as the lipid droplets of HCD-induced hepatic accumulation in the liver tissue, were suppressed by EAT. Taken together, these findings suggest the possibility of developing EAT as a therapeutic agent for improving HCD-induced obesity and hyperlipidemia.

scholarly journals Mixed lineage kinase 3 deficient mice are protected against the high fat high carbohydrate diet-induced steatohepatitis

2013 ◽  
Vol 34 (3) ◽  
pp. 427-437 ◽  
Author(s):  
Samar H. Ibrahim ◽  
Gregory J. Gores ◽  
Petra Hirsova ◽  
Michelle Kirby ◽  
Lili Miles ◽  
...  
Keyword(s):  
High Carbohydrate Diet ◽  
High Fat ◽  
Carbohydrate Diet ◽  
Mixed Lineage Kinase ◽  
High Carbohydrate ◽  
Mixed Lineage Kinase 3 ◽  
Deficient Mice
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