Thyroid-stimulating hormone may participate in insulin resistance by activating toll-like receptor 4 in liver tissues of subclinical hypothyroid rats

Bao, Suqing; Li, Fengbo; Duan, Lijun; Li, Junfeng; Jiang, Xia

doi:10.1007/s11033-023-08834-2

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2024

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Cited by 2 publications

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“…In rodents, GLUT-2 expression occurs in several brain regions, such as the hippocampus, thalamic, hypothalamic, and brain stem nuclei (including the vagal motor nucleus and the nucleus of the tractus solitarius) [ 15 ]. The GLUT-2 protein in the brain regulates the glucose-dependent insulin and glucagon secretion [ 16 ], and in the BLM of proximal tubule cells allows glucose reabsorption from the glomerular filtrate in the kidneys. Knocking out GLUT-2 in mice and humans causes the excretion of filtered glucose in the urine, supporting its glucose reabsorption-stimulating effect.…”

Section: Basic Overview Of Glut-2mentioning

confidence: 99%

Physiological functions of glucose transporter-2: From cell physiology to links with diabetes mellitus

Shen,

Hou,

Zhao

et al. 2024

Heliyon

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Section: Basic Overview Of Glut-2mentioning

confidence: 99%

Physiological functions of glucose transporter-2: From cell physiology to links with diabetes mellitus

Shen,

Hou,

Zhao

et al. 2024

Heliyon

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Oxidative stress in diabetes mellitus and its complications: From pathophysiology to therapeutic strategies

Chen,

Xie,

Feng

et al. 2024

Chinese Medical Journal

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Oxidative stress due to aberrant metabolism is considered as a crucial contributor to diabetes and its complications. Hyperglycemia and hyperlipemia boost excessive reactive oxygen species generation by elevated mitochondrial respiration, increased nicotinamide adenine dinucleotide phosphate oxidase activity, and enhanced pro-oxidative processes, including protein kinase C pathways, hexosamine, polyol, and advanced glycation endproducts, which exacerbate oxidative stress. Oxidative stress plays a significant role in the onset of diabetes and its associated complications by impairing insulin production, increasing insulin resistance, maintaining hyperglycemic memory, and inducing systemic inflammation. A more profound comprehension of the molecular processes that link oxidative stress to diabetes is crucial to new preventive and therapeutic strategies. Therefore, this review discusses the mechanisms underlying how oxidative stress contributes to diabetes mellitus and its complications. We also summarize the current approaches for prevention and treatment by targeting the oxidative stress pathways in diabetes.

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Thyroid-stimulating hormone may participate in insulin resistance by activating toll-like receptor 4 in liver tissues of subclinical hypothyroid rats

Cited by 2 publications

References 49 publications

Physiological functions of glucose transporter-2: From cell physiology to links with diabetes mellitus

Physiological functions of glucose transporter-2: From cell physiology to links with diabetes mellitus

Oxidative stress in diabetes mellitus and its complications: From pathophysiology to therapeutic strategies

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