scholarly journals Gene expression of epithelial glucose transporters: the role of diabetes mellitus.

1994 ◽  
Vol 5 (5) ◽  
pp. S29
Author(s):  
J H Dominguez ◽  
B Song ◽  
L Maianu ◽  
W T Garvey ◽  
M Qulali
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Small Intestine ◽  
High Glucose ◽  
Glucose Transporter ◽  
Basolateral Membrane ◽  
Glucose Levels ◽  
Uncontrolled Diabetes ◽  
Extracellular Level

The functions of absorption of dietary glucose by the small intestine and reabsorption of filtered glucose by the renal proximal tubule are strikingly similar in their organization and in the way they adapt to uncontrolled diabetes mellitus. In both cases, transepithelial glucose and Na+ fluxes are augmented. The epithelial adaptations to hyperglycemia of uncontrolled diabetes are accomplished by increasing the glucose transport surface area and the number of the efflux glucose transporter GLUT2 located in the basolateral membrane. The signals that modify the size of the epithelium and the overexpression of basolateral GLUT2 are not known. It was speculated that high glucose levels and enhanced Na+ flux may be important factors in the signaling event that culminates in a renal and intestinal epithelium that is modified to transport higher rates of glucose against a higher extracellular level of glucose.

scholarly journals The frequency of Tim-3 on circulating Tfh cells was increased in type 2 diabetes mellitus patients

2020 ◽  
Vol 18 ◽  
pp. 205873922098280
Author(s):  
Shuai Guo ◽  
Xujie Yu ◽  
Limei Wang ◽  
Jing Jing ◽  
Yuanyuan Sun ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
High Glucose ◽  
C Peptide ◽  
Glucose Levels ◽  
Tfh Cells ◽  
Fasting Plasma ◽  
Healthy Donors

Type 2 diabetes mellitus (T2DM) is a chronic, low-grade inflammation disease. T follicular helper (Tfh) cells and T cell immunoglobulin and mucin domain 3 (Tim-3) are implicated in many immune diseases. This study aims to explore whether Tim-3 expression on Tfh cells is associated with T2DM progression. White blood cells (WBCs) were harvested from 30 patients with T2DM and 20 healthy donors. The abundance of circulating Tfh cells (cTfh) and the frequency of Tim-3 were analyzed by flow cytometry. Levels of fasting plasma glucose (FPG), insulin, hemoglobin A1C (HbA1C), and fasting plasma C-peptide were measured. Body mass index (BMI) and diabetes duration were also recorded. Patients with T2DM had higher numbers of cTfh cells. In addition, cTfh cells showed a negative correlation with HbA1C and diabetes duration, a positive correlation with fasting plasma C-peptide. The frequency of Tim-3 on cTfh cells was higher among T2DM patients compared with healthy donors. The in vitro experiment showed that high glucose levels increased the abundance cTfh cells but had no effect on Tim-3 expression. Our results suggest that cTfh cells and associated Tim-3 frequency may contribute to the progression of T2DM, and high glucose levels may influence cTfh cells directly.

scholarly journals Role of Melanocortin Signaling in Neuroendocrine and Metabolic Actions of Leptin in Male Rats With Uncontrolled Diabetes

Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4157-4167 ◽  
Author(s):  
Thomas H. Meek ◽  
Miles E. Matsen ◽  
Vincent Damian ◽  
Alex Cubelo ◽  
Streamson C. Chua ◽  
...  
Keyword(s):  
Male Rats ◽  
Melanocortin Receptor ◽  
Glucose Lowering ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Uncontrolled Diabetes ◽  
Streptozotocin Induced Diabetes ◽  
Melanocortin Signaling ◽  
Antidiabetic Effects

Abstract Although the antidiabetic effects of leptin require intact neuronal melanocortin signaling in rodents with uncontrolled diabetes (uDM), increased melanocortin signaling is not sufficient to mimic leptin's glucose-lowering effects. The current studies were undertaken to clarify the role of melanocortin signaling in leptin's ability to correct metabolic and neuroendocrine disturbances associated with uDM. To accomplish this, bilateral cannulae were implanted in the lateral ventricle of rats with streptozotocin-induced diabetes, and leptin was coinfused with varying doses of the melanocortin 3/4 receptor (MC3/4R) antagonist, SHU9119. An additional cohort of streptozotocin-induced diabetes rats received intracerebroventricular administration of either the MC3/4R agonist, melanotan-II, or its vehicle. Consistent with previous findings, leptin's glucose-lowering effects were blocked by intracerebroventricular SHU9119. In contrast, leptin-mediated suppression of hyperglucagonemia involves both melanocortin dependent and independent mechanisms, and the degree of glucagon inhibition was associated with reduced plasma ketone body levels. Increased central nervous system melanocortin signaling alone fails to mimic leptin's ability to correct any of the metabolic or neuroendocrine disturbances associated with uDM. Moreover, the inability of increased melanocortin signaling to lower diabetic hyperglycemia does not appear to be secondary to release of the endogenous MC3/4R inverse agonist, Agouti-related peptide (AgRP), because AgRP knockout mice did not show increased susceptibility to the antidiabetic effects of increased MC3/4R signaling. Overall, these data suggest that 1) AgRP is not a major driver of diabetic hyperglycemia, 2) mechanisms independent of melanocortin signaling contribute to leptin's antidiabetic effects, and 3) melanocortin receptor blockade dissociates leptin's glucose-lowering effect from its action on other features of uDM, including reversal of hyperglucagonemia and ketosis, suggesting that brain control of ketosis, but not blood glucose levels, is glucagon dependent.

Differential role of the vagus in diurnal gene expression rhythms in the small intestine

2004 ◽  
Vol 121 (2) ◽  
pp. 273
Author(s):  
A. Tavakkolizadeh ◽  
A.P. Ramsanahie ◽  
L.L. Levitsky ◽  
M.J. Zinner ◽  
S.W. Ashley ◽  
...  
Keyword(s):  
Gene Expression ◽  
Small Intestine

scholarly journals Glucose transporter gene expression in rat conceptus during high glucose culture

Diabetologia ◽  
1993 ◽  
Vol 36 (8) ◽  
pp. 696-706 ◽  
Author(s):  
Y. Takao ◽  
S. Akazawa ◽  
K. Matsumoto ◽  
H. Takino ◽  
M. Akazawa ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Glucose ◽  
Glucose Transporter ◽  
Transporter Gene

scholarly journals Effect of PGC-1αon Proliferation, Migration, and Transdifferentiation of Rat Vascular Smooth Muscle Cells Induced by High Glucose

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Xiaoqiang Qi ◽  
Yujing Zhang ◽  
Jing Li ◽  
Dongxia Hou ◽  
Yang Xiang
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
High Glucose ◽  
Muscle Cells ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

We assessed the role of PGC-1α (PPARγ coactivator-1 alpha) in glucose-induced proliferation, migration, and inflammatory gene expression of vascular smooth muscle cells (VSMCs). We carried out phagocytosis studies to assess the role of PGC-1α in transdifferentiation of VSMCs by flow cytometry. We found that high glucose stimulated proliferation, migration and inflammatory gene expression of VSMCs, but overexpression of PGC-1α attenuated the effects of glucose. In addition, overexpression of PGC-1α decreased mRNA and protein level of VSMCs-related genes, and induced macrophage-related gene expression, as well as phagocytosis of VSMCs. Therefore, PGC-1α inhibited glucose-induced proliferation, migration and inflammatory gene expression of VSMCs, which are key features in the pathology of atherosclerosis. More importantly, PGC-1α transdifferentiated VSMCs to a macrophage-like state. Such transdifferentiation possibly increased the portion of VSMCs-derived foam cells in the plaque and favored plaque stability.

scholarly journals Role of p90RSK in regulating the Crabtree effect: implications for cancer

2013 ◽  
Vol 41 (1) ◽  
pp. 124-126 ◽  
Author(s):  
Emily K. Redman ◽  
Paul S. Brookes ◽  
Marcin K. Karcz
Keyword(s):  
Cancer Cell ◽  
High Glucose ◽  
Cell Metabolism ◽  
Cell Signalling ◽  
Cell Types ◽  
Crabtree Effect ◽  
Glucose Levels ◽  
Mitogen Activated Protein ◽  
Ribosomal S6 Kinase

High glucose inhibits mitochondrial respiration, known as the ‘Crabtree effect’, in cancer cells and possibly other cell types. The upstream pathways regulating this phenomenon are poorly understood. In diabetes, where glucose levels are elevated, the p90RSK (p90 ribosomal S6 kinase) has received much attention as a potential upstream mediator of the effects of high glucose. Evidence is also emerging that p90RSK may play a role in cancer cell signalling, although the role of p90RSK in regulating cancer cell metabolism is unclear. In the present paper, we provide an overview of the Crabtree effect and its relationship to mitochondrial metabolism. Furthermore, preliminary data are presented suggesting a role for p90RSK and its upstream components, the ERK (extracellular-signal-regulated kinase) family of MAPKs (mitogen-activated protein kinases), in the Crabtree effect.

scholarly journals Glucose Uptake in Trichoderma harzianum: Role of gtt1

2003 ◽  
Vol 2 (4) ◽  
pp. 708-717 ◽  
Author(s):  
Jesús Delgado-Jarana ◽  
Miguel Ángel Moreno-Mateos ◽  
Tahía Benítez
Keyword(s):  
Gene Expression ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Trichoderma Harzianum ◽  
Glucose Transporter ◽  
Biochemical Characterization ◽  
Carbon Sources ◽  
Low Carbon ◽  
Filamentous Ascomycete

ABSTRACT Using a differential display technique, the gene gtt1, which codes for a high-affinity glucose transporter, has been cloned from the mycoparasite fungus Trichoderma harzianum CECT 2413. The deduced protein sequence of the gtt1 gene shows the 12 transmembrane domains typical of sugar transporters, together with certain residues involved in glucose uptake, such as a conserved arginine between domains IV and V and an aromatic residue (Phe) in the sequence of domain X. The gtt1 gene is transcriptionally regulated, being repressed at high levels of glucose. When carbon sources other than glucose are utilized, gtt1 repression is partially alleviated. Full derepression of gtt1 is obtained when the fungus is grown in the presence of low carbon source concentrations. This regulation pattern correlates with the role of this gene in glucose uptake during carbon starvation. Gene expression is also controlled by pH, so that the gtt1 gene is repressed at pH 6 but not at pH 3, a fact which represents a novel aspect of the influence of pH on the gene expression of transporters. pH also affects glucose transport, since a strongly acidic pH provokes a 40% decrease in glucose transport velocity. Biochemical characterization of the transport shows a very low Km value for glucose (12 μM). A transformant strain that overexpresses the gtt1 gene shows a threefold increase in glucose but not galactose or xylose uptake, a finding which confirms the role of the gtt1 gene in glucose transport. The cloning of the first filamentous ascomycete glucose transporter is the first step in elucidating the mechanisms of glucose uptake and carbon repression in aerobic fungi.

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