Control of liver glucokinase activity: A potential new target for incretin hormones?

Francini, Flavio; Massa, María Laura; Polo, Mónica Patricia; Villagarcía, Hernán Gonzalo; Castro, M.; Gagliardino, Juan José

doi:10.1016/j.peptides.2015.10.006

Cited by 7 publications

(7 citation statements)

References 44 publications

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“…In one study, low fructose (7%) content in drinking water was sufficient to cause glucose intolerance with abnormal morphology and function of pancreatic islet cells in Wistar rats, but without changes in FBG, insulin and lipids levels 144 . However, in another study, the same strain of rats fed with fructose‐rich diet (10% w/v in drinking water) developed hypertriglyceridaemia and a state of insulin resistance (demonstrated by hyperinsulinaemia with normoglycaemia, high insulin:glucose molar ratio and HOMA‐IR index) after 3 weeks of fructose administration 145 …”

Section: Diet‐induced Rodent Modelsmentioning

confidence: 98%

“…144 However, in another study, the same strain of rats fed with fructose-rich diet (10% w/v in drinking water) developed hypertriglyceridaemia and a state of insulin resistance (demonstrated by hyperinsulinaemia with normoglycaemia, high insulin:glucose molar ratio and HOMA-IR index) after 3 weeks of fructose administration. 145 HFHSD is also commonly used to experimentally replicate prediabetes. 146,147 Different sources and amounts of CHO (mainly fructose or sucrose) and fats have been used.…”

Section: Prediabetesmentioning

confidence: 99%

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Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

et al. 2020

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Diet is a critical element determining human health and diseases, and unbalanced food habits are major risk factors for the development of obesity and related metabolic disorders. Despite technological and pharmacological advances, as well as intensification of awareness campaigns, the prevalence of metabolic disorders worldwide is still increasing. Thus, novel therapeutic approaches with increased efficacy are urgently required, which often depends on cellular and molecular investigations using robust animal models. In the absence of perfect rodent models, those induced by excessive consumption of fat and sugars better replicate the key aspects that are the root causes of human metabolic diseases. However, the results obtained using these models cannot be directly compared, particularly because of the use of different dietary protocols, and animal species and strains, among other confounding factors. This review article revisits diet-induced models of obesity and related metabolic disorders, namely, metabolic syndrome, prediabetes, diabetes and nonalcoholic fatty liver disease. A critical analysis focused on the main pathophysiological features of rodent models, as opposed to the criteria defined for humans, is provided as a practical guide with a translational perspective for the establishment of animal models of obesity-related metabolic diseases.

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Section: Diet‐induced Rodent Modelsmentioning

confidence: 98%

Section: Prediabetesmentioning

confidence: 99%

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

et al. 2020

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“…Number of reported literatures have demonstrated that Sita can increases the GLP-1 level in the brain along with improve the cognitive behaviors in rat model of AD (Civantos et al, 2017). While in another investigation Sita has likewise increases the neuroprotective effect of pregabalin against pentylenetetrazole (PTZ)-induced epilepsy in mice through its effect on OS, apoptosis, and autophagic pathways (Francini et al, 2015;Kazmi, Afzal, Gupta, & Anwar, 2012). Quercetin is flavonol, type of flavonoid found in apples, dark tea, and so forth (Dave, Shukla, Wala, & Pillai, 2019).…”

mentioning

confidence: 99%

Activation of Nrf2 signaling by sitagliptin and quercetin combination against β‐amyloid induced Alzheimer's disease in rats

Tian

et al. 2019

Drug Development Research

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The objective of this study was to evaluate the neuroprotective effect of sitagliptin (Sita), quercetin (QCR) and its combination in β‐amyloid (Aβ) induced Alzheimer's disease (AD). Male Sprague–Dawley rats, weighing between 220 and 280 g were used for experiment. Rats were divided into 5 groups (n = 10) and the groups were as follows: (a) Sham control; (b) Aβ injected; (c) Aβ injected + Sita 100; (d) Aβ injected + QCR 100; and (e) Aβ injected + Sita 100 + QCR 100. Cognitive performance was observed by the Morris water maze (MWM), biochemical markers, for example, MDA, SOD, CAT, GSH, Aβ1‐42 level, Nrf2/HO‐1 expression and histopathological study of rat brain were estimated. Pretreatment with Sita, QCR and their combination showed a significant increase in escape latency in particular MWM cognitive model. Further co‐administration of sita and QCR significantly reduced Aβ1‐42 level when compared with individual treatment. Biochemical markers, for example, increased SOD, CAT and GSH, decreased MDA were seen, and histopathological studies revealed the reversal of neuronal damage in the treatment group. Additionally, Nrf2/HO‐1 pathway in rat's brain was significantly increased by Sita, QCR and their combination. Pretreatment with QCR potentiates the action of Sita in Aβ induced AD in rats. The improved cognitive memory could be because of the synergistic effect of the drugs by decreasing Aβ1‐42 level, antioxidant activity and increased expression of Nrf2/HO‐1 in rat brain.

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“…GLK is dimeric with 321 amino acids and an approximate molecular weight of 35 kDa, and it is a crucial enzyme in regulating glc utilization in vivo as part of the initial steps of glycolysis . Found principally in the liver, its deregulation, caused either by genetic or environmental factors, can cause severe problems, such as diabetes; conversely, it is a target of interest for treating various forms of diabetes. , Though not strictly following a MM kinetic process, the GLK enzyme is not product inhibited and can be adequately described by MM for ATP consumption. , The GLK reaction was first tested by a coupled assay, the downstream production of NADH from NAD by glucose-6-phosphate dehydrogenase (6-PGDH) . Upon confirmation of GLK activity in the experimental conditions, the QD-Tb assays were realized.…”

Section: Resultsmentioning

confidence: 99%

“…38 Found principally in the liver, its deregulation, caused either by genetic or environmental factors, can cause severe problems, such as diabetes; conversely, it is a target of interest for treating various forms of diabetes. 39,40 Though not strictly following a MM kinetic process, the GLK enzyme is not product inhibited and can be adequately described by MM for ATP consumption. 41,42 The GLK reaction was first tested by a coupled assay, the downstream production of NADH from NAD by glucose-6-phosphate dehydrogenase (6-PGDH).…”

Section: Acs Applied Nano Materialsmentioning

confidence: 99%

Quantum Dots as Förster Resonance Energy Transfer Acceptors of Lanthanides in Time-Resolved Bioassays

Dı́az¹,

Lasarte‐Aragonés

Lowery

et al. 2018

ACS Appl. Nano Mater.

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We report a flexible and modular design for biosensors based on exploiting semiconductor quantum dots (QDs) and their excellent Forster resonance energy transfer (FRET) acceptor properties along with the long-lived fluorescent lifetimes of lanthanide donors. We demonstrate the format's wide application by developing a broad adenosine diphosphate (ADP) sensor with quantitative and highthroughput capabilities as a kinase/ATPase assay method. The sensor is based on a Terbium (Tb)-labeled antibody (Ab) that selectively recognizes ADP versus ATP. The Tb-labeled Ab (Ab-Tb) acts as a FRET donor to a QD, which has an ADP modified His 6 -peptide conjugated to its surface via metal-affinity coordination. This strategy of using self-assembly, modified peptides to present antibody epitopes on QD surfaces is readily transferable to other assays of interest. We utilize time-resolved FRET (TR-FRET) to measure the amounts of Ab-Tb bound to the QD by looking at the emission ratio of the QD and Tb in a time-gated manner, minimizing background signal. With the addition of free ADP the antibody is competitively separated from the QD and a change in the ratiometric emission signal correlates with the free ADP concentration. The sensor obtained a detection limit below 10 nM of free ADP and quantitation limit of 35 nM ADP using 8 nM of sensor. Quantitative values were obtained for a model enzyme (glucokinase) kinetics, as well as demonstrations of the assays capability to distinguish enzyme inhibitors. We discuss future outlooks and note areas for improvement in similar design strategies.

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Control of liver glucokinase activity: A potential new target for incretin hormones?

Cited by 7 publications

References 44 publications

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

Activation of Nrf2 signaling by sitagliptin and quercetin combination against β‐amyloid induced Alzheimer's disease in rats

Quantum Dots as Förster Resonance Energy Transfer Acceptors of Lanthanides in Time-Resolved Bioassays

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