Mechanism of glucose sensing in the small intestine

2003 ◽  
Vol 31 (6) ◽  
pp. 1140-1142 ◽  
Author(s):  
J. Dyer ◽  
S. Vayro ◽  
S.P. Shirazi-Beechey
Keyword(s):  
Glucose Transporter ◽  
Glucose Sensor ◽  
Cell Function ◽  
Glucose Sensing ◽  
Model Systems ◽  
Luminal Membrane ◽  
Sense And Respond ◽  
Vitro Model

Sensing nutrients is a fundamental task for all living cells. For most eukaryotic cells glucose is a major source of energy, having significant and varied effects on cell function. Interest in identifying mechanisms by which cells sense and respond to variations in glucose concentration has increased recently. The epithelial cells lining the intestinal tract are exposed, from the luminal domain, to an environment with continuous and massive fluctuations in the levels of dietary monosaccharides. Enterocytes therefore have to sense and respond to the significant changes in the levels of luminal sugars, and regulate the expression of the intestinal glucose transporter (Na+/glucose co-transporter, SGLT1) accordingly. Our data, using a combination of in vivo and in vitro model systems, suggest that glucose in the lumen of the intestine is sensed by a glucose sensor residing on the external face of the enterocyte luminal membrane. Glucose binds to the sensor and generates an intracellular signal leading to enhancement in the expression of SGLT1. The generated signal is independent of glucose metabolism and is likely to operate via a G-protein-coupled receptor and cAMP/protein kinase A signalling cascade.

Glucose homeostasis and hypothalamic-pituitary-adrenocortical axis during development in rats

1990 ◽  
Vol 259 (5) ◽  
pp. E601-E613 ◽  
Author(s):  
E. P. Widmaier
Keyword(s):  
Stress Responses ◽  
Adrenocorticotropic Hormone ◽  
Glucose Sensor ◽  
Adult Life ◽  
Glucose Sensing ◽  
Physiological Data ◽  
Compensatory Mechanisms ◽  
Definition Of

Glucoprivation represents a model stress in which activation of different stress responses at different ages can be monitored both in vivo and in vitro. Physiological data indicate rat brain contains a liver/pancreas-type glucose sensor, yet no biochemical or immunocytochemical evidence exists for such a sensor. Young rats appear to lack normal hypothalamic glucose-sensing ability and do not show typical secretory patterns of corticotropin-releasing factor, adrenocorticotropic hormone, or corticosterone after experimentally induced glucoprivation. However, they hypersecrete catecholamines and glucagon (compared with adults) and thrive on fuel sources other than glucose that are abundant after birth. High steroid levels during the first 24 h after birth may be critical for inducing gluconeogenic enzymes and promoting differentiation of tissues like pancreas. Neonatal rats also have unique control systems to combat the damaging effects of other stresses like hypoxia; these systems may disappear in adults. Thus the definition of stress may change during development, and the compensatory mechanisms employed to combat stress change from neonatal to adult life and are intricately related to the metabolic needs of the animal.

scholarly journals In vitro Characterization of Insulin−Producing β-Cell Spheroids

2021 ◽  
Vol 8 ◽  
Author(s):  
Yonela Ntamo ◽  
Ebrahim Samodien ◽  
Joleen Burger ◽  
Nolan Muller ◽  
Christo J. F. Muller ◽  
...  
Keyword(s):  
Glucose Utilization ◽  
Cell Function ◽  
3D Culture ◽  
Glucose Sensing ◽  
Blue Staining ◽  
Cell Physiology ◽  
Β Cell ◽  
3D Spheroids

Over the years, immortalized rodent β-cell lines such as RIN, HIT, MIN, βTC, and INS-1 have been used to investigate pancreatic β-cell physiology using conventional two-dimensional (2D) culture techniques. However, physical and physiological limitations inherent to 2D cell culture necessitates confirmatory follow up studies using sentient animals. Three-dimensional (3D) culture models are gaining popularity for their recapitulation of key features of in vivo organ physiology, and thus could pose as potential surrogates for animal experiments. In this study, we aimed to develop and characterize a rat insulinoma INS-1 3D spheroid model to compare with 2D monolayers of the same cell line. Ultrastructural verification was done by transmission electron microscopy and toluidine blue staining, which showed that both 2D monolayers and 3D spheroids contained highly granulated cells with ultrastructural features synonymous with mature pancreatic β-cells, with increased prominence of these features observed in 3D spheroids. Viability, as assessed by cellular ATP quantification, size profiling and glucose utilization, showed that our spheroids remained viable for the experimental period of 30 days, compared to the limiting 5-day passage period of INS-1 monolayers. In fact, increasing ATP content together with spheroid size was observed over time, without adverse changes in glucose utilization. Additionally, β-cell function, assessed by determining insulin and amylin secretion, showed that the 3D spheroids retained glucose sensing and insulin secretory capability, that was more acute when compared to 2D monolayer cultures. Thus, we were able to successfully demonstrate that our in vitro INS-1 β-cell 3D spheroid model exhibits in vivo tissue-like structural features with extended viability and lifespan. This offers enhanced predictive capacity of the model in the study of metabolic disease, β-cell pathophysiology and the potential treatment thereof.

scholarly journals Imaging cell biology in live animals: Ready for prime time

2013 ◽  
Vol 201 (7) ◽  
pp. 969-979 ◽  
Author(s):  
Roberto Weigert ◽  
Natalie Porat-Shliom ◽  
Panomwat Amornphimoltham
Keyword(s):  
Cell Biology ◽  
Cancer Biology ◽  
In Vitro Model ◽  
Time Lapse ◽  
Living Cells ◽  
Model Systems ◽  
Prime Time ◽  
Vitro Model

Time-lapse fluorescence microscopy is one of the main tools used to image subcellular structures in living cells. Yet for decades it has been applied primarily to in vitro model systems. Thanks to the most recent advancements in intravital microscopy, this approach has finally been extended to live rodents. This represents a major breakthrough that will provide unprecedented new opportunities to study mammalian cell biology in vivo and has already provided new insight in the fields of neurobiology, immunology, and cancer biology.

Biological Responses of Fibroblasts to Cyclic Stretching: A Novel Culture Model Study

2000 ◽  
Author(s):  
James H.-C. Wang ◽  
David Stone ◽  
Fengyan Jia ◽  
Chris Celechovsky ◽  
Savio L.-Y. Woo
Keyword(s):  
Control Cell ◽  
Model Systems ◽  
Cell Alignment ◽  
Experimental Conditions ◽  
Cyclic Stretching ◽  
Biological Responses ◽  
Model Study ◽  
Vitro Model

Abstract Because of the advantage of better control of experimental conditions, in vitro model systems have been developed to examine the effects of mechanical loading on cells. Previous studies have shown that cyclic stretching causes cells to change orientation, proliferation and gene expression (Buck et al., 1980; Wang et al., 1995; Leung et al., 1976). However, one drawback of these model systems is that they are unable to control cell alignment and shape, and in addition, some provide heterogeneous strains to cells during stretching (See review by Schaffer, 1994). Consequently, cellular responses in these systems may not be similar to those in vivo. For example, tendon and ligament fibroblasts align with collagen fibers in vivo and are hence subjected to stretching along the tissue long axis. In contrast, in many existing systems, cells either randomly orient or orient away from the stretching direction.

scholarly journals Persistent organic pollutants and obesity: are they potential mechanisms for breast cancer promotion?

2015 ◽  
Vol 22 (2) ◽  
pp. R69-R86 ◽  
Author(s):  
Denise K Reaves ◽  
Erika Ginsburg ◽  
John J Bang ◽  
Jodie M Fleming
Keyword(s):  
Breast Cancer ◽  
Organic Pollutants ◽  
Persistent Organic Pollutants ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Causal Link ◽  
Model Systems ◽  
Tissue Microenvironment

Dietary ingestion of persistent organic pollutants (POPs) is correlated with the development of obesity. Obesity alters metabolism, induces an inflammatory tissue microenvironment, and is also linked to diabetes and breast cancer risk/promotion of the disease. However, no direct evidence exists with regard to the correlation among all three of these factors (POPs, obesity, and breast cancer). Herein, we present results from current correlative studies indicating a causal link between POP exposure through diet and their bioaccumulation in adipose tissue that promotes the development of obesity and ultimately influences breast cancer development and/or progression. Furthermore, as endocrine disruptors, POPs could interfere with hormonally responsive tissue functions causing dysregulation of hormone signaling and cell function. This review highlights the critical need for advancedin vitroandin vivomodel systems to elucidate the complex relationship among obesity, POPs, and breast cancer, and, more importantly, to delineate their multifaceted molecular, cellular, and biochemical mechanisms. Comprehensivein vitroandin vivostudies directly testing the observed correlations as well as detailing their molecular mechanisms are vital to cancer research and, ultimately, public health.

Synergy between paclitaxel plus an exogenous methyl donor in the suppression of murine demyelinating diseases

2007 ◽  
Vol 13 (5) ◽  
pp. 596-609 ◽  
Author(s):  
FG Mastronardi ◽  
H. Tsui ◽  
S. Winer ◽  
DD Wood ◽  
T. Selvanantham ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Combination Therapy ◽  
Clinical Signs ◽  
Demyelinating Diseases ◽  
Model Systems ◽  
Methyl Donor ◽  
Negative Balance ◽  
Vitro Model

Progressive demyelination in multiple sclerosis (MS) reflects the negative balance between myelin damage and repair due to physical and molecular barriers, such as astrocytic glial scars, between oligodendrocytes and target neurons. In this paper, we show that combination therapy with paclitaxel (Taxol®) plus the universal methyl-donor, vitamin B12CN (B12CN), dramatically limits progressive demyelination, and enhances remyelination in several independent, immune and nonimmune, in vivo and in vitro model systems. Combination therapy significantly reduced clinical signs of EAE in SJL mice, as well as the spontaneously demyelinating ND4 transgenic mouse. Astrocytosis was normalised in parallel to ultrastructural and biochemical evidence of remyelination. The combination therapy suppressed T cell expansion, reduced IFN-gamma, while enhancing IFN-beta and STAT-1 expression, STAT-1 phosphorylation and methylation of STAT-1 and MBP in the brain. Paclitaxel/B12CN has nearly identical effects to the previously described combination of IFN-beta/ B12CN, whose clinical usefulness is transient because of IFN-neutralising antibodies, not observed (or expected) with the present drug combination. This report provides a mechanistic foundation for the development of a new therapeutic strategy in humans with MS. Multiple Sclerosis 2007; 13: 596-609. http://msj.sagepub.com

scholarly journals Author Correction: The promise(s) of mesenchymal stem cell therapy in averting preclinical diabetes: lessons from in vivo and in vitro model systems

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nagasuryaprasad Kotikalapudi ◽  
Samuel Joshua Pragasam Sampath ◽  
Sinha Sukesh Narayan ◽  
Bhonde R. ◽  
Harishankar Nemani ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Cell Therapy ◽  
In Vitro Model ◽  
Model Systems ◽  
Mesenchymal Stem Cell Therapy ◽  
Preclinical Diabetes ◽  
Vitro Model

Morphological effects of sulfur mustard on a human skin equivalent

1991 ◽  
Vol 49 ◽  
pp. 78-79
Author(s):  
J.P. Petrali ◽  
S.B. Oglesby ◽  
T.A. Justus
Keyword(s):  
Human Skin ◽  
Sulfur Mustard ◽  
Athymic Nude Mouse ◽  
Skin Equivalent ◽  
Model Systems ◽  
Cells In Culture ◽  
Vitro Model ◽  
Human Skin Equivalent

We have previously reported morphological correlates of sulfur mustard (HD) toxicity in several model systems: the human skin grafted athymic nude mouse; the hairless guinea pig; and human cells in culture. We are now describing HD effects in a human skin equivalent, TESTSKIN®, and comparing these effects with those already reported for animal models and cells in culture. The human skin equivalent (HSE) is used here as an organotypic in vitro model system to bridge the knowledge gap between HD effects in monotypic cells in culture and animal in vivo effects. Additionally, HSE allowed study of HD toxicity which circumvented the concern of using human biopsied tissue.

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