Chronic hyperglycemia mediated physiological alteration and metabolic distortion leads to organ dysfunction, infection, cancer progression and other pathophysiological consequences: An update on glucose toxicity

Giri, Biplab; Dey, Sananda; Das, Tanaya; Sarkar, Mrinmoy; Banerjee, Jhimli; Dash, Sandeep Kumar

doi:10.1016/j.biopha.2018.07.157

Cited by 310 publications

(229 citation statements)

References 325 publications

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“…Postprandial glycemic control is notably important for healthy subjects, particularly as related to preventing diabetes, obesity, and cardiovascular diseases. As such, the obtained results could serve for optimizing glycemic control in both healthy and hospitalized individuals, thereby attenuating the risks associated to obesity, diabetes, cancer, cardiovascular disease, infection, wound healing, or other organ dysfunctions (Giri et al, 2018).…”

Section: R a F Tmentioning

confidence: 99%

“…Postprandial glycemic control is notably important for healthy subjects, particularly as related to preventing diabetes, obesity, and cardiovascular diseases. In addition, this could be particularly useful for the clinical community, since maintained hyperglycemia provokes insulin resistance, a pro-inflammatory environment, and high oxidative stress (Giri et al, 2018). Indeed, cardiovascular risks increase progressively with postprandial glycemia levels (characterized by a rapid, large and sustained increase in blood glucose levels), negatively impacting their evolution, especially for non-diabetic patients (Hsu, 2012).…”

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confidence: 99%

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Effect of neuromuscular electrical stimulation frequency on postprandial glycemia, current-related discomfort, and muscle soreness. A crossover study

Guzmán-González

Llanos

Calatayud

et al. 2019

Appl. Physiol. Nutr. Metab.

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Consensus is lacking regarding optimal neuromuscular electrical stimulation (NMES) parameters for postprandial glycemic control. Therefore, the aim of this study was to determine the NMES frequency inducing the greatest hypoglycemic effect in healthy individuals. The secondary aim was to compare current-related discomfort and muscle soreness between different frequencies. We conducted an experimental clinical study with a randomized crossover design. Sixteen healthy and sedentary participants received NMES for 20 min at 5, 10, or 50 Hz (pulse duration: 400 μs, on-off ratio: 4:12 s) following a standardized meal. Glycemia, discomfort, and muscle soreness during and after NMES were compared between conditions. Five-hertz NMES generated a significant hypoglycemic effect, contrary to 10 Hz and 50 Hz. Ten-hertz and 50-Hz NMES resulted respectively in lower current-related discomfort and greater muscle soreness compared with the other frequencies. Women reported higher discomfort than men. These findings contribute towards the possibility of more efficient long-term NMES treatments in terms of glycemic response and patient tolerance.

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Section: R a F Tmentioning

confidence: 99%

mentioning

confidence: 99%

Effect of neuromuscular electrical stimulation frequency on postprandial glycemia, current-related discomfort, and muscle soreness. A crossover study

Guzmán-González

Llanos

Calatayud

et al. 2019

Appl. Physiol. Nutr. Metab.

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“…57 We found that diabetes in lean STZ-treated mice promotes oxidative stress-related changes in the SN and CPu, in agreement with the well-documented association between hyperglycemia and oxidative stress. 28,58,59 Because of the relatively high-energy demands that they require for function, 44,60 nigrostriatal dopaminergic neurons are particularly vulnerable to oxidative stress, [61][62][63] which, in turn, is thought to play an important role in PD. 44,64,65 Notably, 6-OHDA used at a subthreshold dose did not produce detectable motor impairment in nondiabetic animals despite significant decreases in TH (42%) and DAT (36%) in the striatum, in line with previous studies.…”

Section: I a B E T E Smentioning

confidence: 99%

Diabetes Causes Dysfunctional Dopamine Neurotransmission Favoring Nigrostriatal Degeneration in Mice

et al. 2020

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Background Numerous studies indicate an association between neurodegenerative and metabolic diseases. Although still a matter of debate, growing evidence from epidemiological and animal studies indicate that preexisting diabetes increases the risk to develop Parkinson's disease. However, the mechanisms of such an association are unknown. Objectives We investigated whether diabetes alters striatal dopamine neurotransmission and assessed the vulnerability of nigrostriatal neurons to neurodegeneration. Methods We used streptozotocin‐treated and genetically diabetic db/db mice. Expression of oxidative stress and nigrostriatal neuronal markers and levels of dopamine and its metabolites were monitored. Dopamine release and uptake were assessed using fast‐scan cyclic voltammetry. 6‐Hydroxydopamine was unilaterally injected into the striatum using stereotaxic surgery. Motor performance was scored using specific tests. Results Diabetes resulted in oxidative stress and decreased levels of dopamine and its metabolites in the striatum. Levels of proteins regulating dopamine release and uptake, including the dopamine transporter, the Girk2 potassium channel, the vesicular monoamine transporter 2, and the presynaptic vesicle protein synaptobrevin‐2, were decreased in diabetic mice. Electrically evoked levels of extracellular dopamine in the striatum were enhanced, and altered dopamine uptake was observed. Striatal microinjections of a subthreshold dose of the neurotoxin 6‐hydroxydopamine in diabetic mice, insufficient to cause motor alterations in nondiabetic animals, resulted in motor impairment, higher loss of striatal dopaminergic axons, and decreased neuronal cell bodies in the substantia nigra. Conclusions Our results indicate that diabetes promotes striatal oxidative stress, alters dopamine neurotransmission, and increases vulnerability to neurodegenerative damage leading to motor impairment. © 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

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“…Proper blood glucose homeostasis is essential for a healthy life and prolonged hyperglycemia can increase risk of diabetes mellitus, cardiovascular disease, and kidney disease. [16][17][18] Pancreatic β-cells sense changes in blood glucose levels and, under conditions of elevated circulating glucose, release insulin via Ca 2+ -dependent exocytosis. 19 NNAT was first discovered in β-cells in 1997, 13 however, much of what we know on its physiological role has only recently surfaced.…”

Section: Glucose Homeostasismentioning

confidence: 99%

Neuronatin regulates whole‐body metabolism: is thermogenesis involved?

Braun¹,

Geromella²,

Hamstra³

et al. 2020

FASEB BioAdvances

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The neuronatin (NNAT, 3.9 kb) gene is paternally inherited with the maternal allele silenced via DNA methylation. 1,2 Genomic imprinting such as this results in monoallelic expression-a characteristic of several other genes critical for growth, development, and metabolism. 3 Through alternative splicing, NNAT mRNA produces two isoforms, NNATα (81 amino acids) and NNATβ (54 amino acids), 4,5 though the extent with which these isoforms are functionally redundant or divergent remain to be uncovered. NNAT/Nnat mRNA is enriched in the developing brain, and while downregulated

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Chronic hyperglycemia mediated physiological alteration and metabolic distortion leads to organ dysfunction, infection, cancer progression and other pathophysiological consequences: An update on glucose toxicity

Cited by 310 publications

References 325 publications

Effect of neuromuscular electrical stimulation frequency on postprandial glycemia, current-related discomfort, and muscle soreness. A crossover study

Effect of neuromuscular electrical stimulation frequency on postprandial glycemia, current-related discomfort, and muscle soreness. A crossover study

Diabetes Causes Dysfunctional Dopamine Neurotransmission Favoring Nigrostriatal Degeneration in Mice

Neuronatin regulates whole‐body metabolism: is thermogenesis involved?

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