Endocrine characteristics and risk factors of type 2 diabetes complicated with gastrointestinal autonomic neuropathy: A single-center retrospective study

Guan, Wei; Li, Shan; Sun, Wenzao; Kang, Yuqin; Li, Xiaoqin

doi:10.1097/md.0000000000033467

Cited by 3 publications

(3 citation statements)

References 18 publications

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“…Individuals with obesity produce insulin resistance in their adipose tissue, which induces increased insulin secretion from pancreatic β-cells. However, this overcompensation for insulin secretion can lead to pancreatic β-cell failure and inadequate insulin secretion, ultimately resulting in non-insulin-dependent diabetes mellitus [15]. The pathogenesis of this correlation between obesity and non-insulin-dependent diabetes mellitus has been studied extensively.…”

Section: Disease Causality Discovery Resultsmentioning

confidence: 99%

A study on large-scale disease causality discovery from biomedical literature*

yu,

Dong,

et al. 2024

Preprint

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Background With the increasing amount of scientific and technical literature available, it has posed difficulties for deeper knowledge discovery. Biomedical semantic relationship extraction can reveal important biomedical entities and the semantic relationships between them, which is an important basis for biomedical knowledge discovery, clinical decision making and other applications. Identifying the causative relationships of diseases is a significant research field, which can help speed up the discovery of underlying mechanisms of diseases and promote better prevention and treatment of diseases. Methods This study aims to optimize the automatic extraction of disease causality of SemRep tool by constructing a semantic predicate vocabulary that specifically conveys disease causality, allowing for the discovery of disease causality within the biomedical literature. We extracted semantic feature words based on existing research and the parsing and recognition results of literature using SemRep. We then filtered and evaluated textual semantic predicates according to the semantic feature words and constructed a semantic predicate vocabulary expressing disease causality. Results By improving the automatic extraction of disease causality pairs, the proposed method would facilitate better disease causality mining from biomedical literature. We constructed a semantic predicate vocabulary expressing disease causality using 50 predicates with an accuracy of at least 40%. Conclusions The approach of using optimized semantic predicates to discover disease causality from large-scale biomedical literature is feasible. It can provide insights for the extraction of other types of semantic relationships and for machine learning methods as well, thus contributing to the discovery and exploitation of disease causality knowledge and supporting clinical diagnosis and disease prevention and control.

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Section: Disease Causality Discovery Resultsmentioning

confidence: 99%

A study on large-scale disease causality discovery from biomedical literature*

yu,

Dong,

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…ACTH is the main secretory hormone of glucocorticoids, which can lead to insulin resistance directly [56] or through different pathways, such fatty acid accumulation [57], desensitisation of insulin receptors and decreased insulin-mediated expression of glucose transporter in the membrane [58]. Abnormal levels of ACTH are associated with insulin resistance in many patients with metabolic conditions [59], demonstrating the clinical relevance of HPA axis disruption in metabolic changes. In the present study, metabolomics analysis shown decreased nucleotide synthesis and, although not significant, a trend for impaired pentose phosphate pathway activity (PPP) in the serum of ACTH-treated animals.…”

Section: Discussionmentioning

confidence: 99%

The role of IL-6 in dopamine dysregulation underlying anhedonia phenotype in rats

Varela,

Macpherson,

Houghton

et al. 2023

Preprint

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AimsTo investigate the role of peripheral metabolic change and chronic low-grade inflammation on striatal dopamine dynamics and anhedonia-like behaviour induced by hypothalamic–pituitary–adrenal (HPA) axis disruption.MethodsWistar rats were trained in a progressive-ratio/concurrent effort-related choice paradigm to assess effort-related decision making. After reaching a stable baseline, animals received daily injections of adrenocorticotrophic hormone (ACTH) or saline for 24 days. On the 23rdand 24thday, animals received a bupropion challenge (10mg/kg and 20mg/kg respectively) 30 minutes prior to the behavioural testing session. On the 25thday, animals received a single injection of bupropion (20mg/kg) 30 minutes prior to euthanasia. Peripheral and central inflammatory markers were assessed through ELISA and In-Cell Western assay; glucose transport activity was assessed in peripheral blood mononuclear cells though a commercial assay kit; brain levels of dopaminergic and inflammatory markers were assessed in the nucleus accumbens (NAc) and prefrontal cortex (PFC) through immunohistochemistry; and serum central carbon metabolism metabolites were assessed through a metabolomics approach.ResultsACTH induced an anhedonia-like phenotype, decreased tyrosine hydroxylase (TH) levels in the NAc, increased peripheral IL-6 levels, and decreased glucose transport activity and glucose metabolites when compared to control group. Bupropion treatment was not able to reverse the anhedonic phenotype. Glucose uptake was positively correlated to behaviour; TH levels were correlated to microglia volume; metabolites were correlated to TH levels; and IL6 was correlated to TH levels and metabolites.ConclusionChronic ACTH treatment can induce treatment-resistant anhedonia in rats, and the interaction between peripheral immunometabolic state and central dopamine synthesis is a potential mechanism underlying this phenotype.

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“…This condition in type 2 diabetes forms part of broader metabolic dysfunction, including changes in gut microbiota, increased intestinal permeability, and chronic low-grade inflammation[ 24 , 29 - 31 ]. Moreover, lifestyle factors, notably dietary habits and physical activity, play a significant role in type 2 diabetes, influencing the severity and progression of enteric neuropathy[ 32 ]. Modifiable risk factors such as diet and exercise are thus crucial in managing GI complications in diabetic patients[ 28 , 33 , 34 ].…”

Section: Introductionmentioning

confidence: 99%

Enteric neuropathy in diabetes: Implications for gastrointestinal function

Abdalla

2024

World J Gastroenterol

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Diabetes, commonly known for its metabolic effects, also critically affects the enteric nervous system (ENS), which is essential in regulating gastrointestinal (GI) motility, secretion, and absorption. The development of diabetes-induced enteric neuropathy can lead to various GI dysfunctions, such as gastroparesis and irregular bowel habits, primarily due to disruptions in the function of neuronal and glial cells within the ENS, as well as oxidative stress and inflammation. This editorial explores the pathophysiological mechanisms underlying the development of enteric neuropathy in diabetic patients. Additionally, it discusses the latest advances in diagnostic approaches, emphasizing the need for early detection and intervention to mitigate GI complications in diabetic individuals. The editorial also reviews current and emerging therapeutic strategies, focusing on pharmacological treatments, dietary management, and potential neuromodulatory interventions. Ultimately, this editorial highlights the necessity of a multidisciplinary approach in managing enteric neuropathy in diabetes, aiming to enhance patient quality of life and address a frequently overlooked complication of this widespread disease.

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Endocrine characteristics and risk factors of type 2 diabetes complicated with gastrointestinal autonomic neuropathy: A single-center retrospective study

Cited by 3 publications

References 18 publications

A study on large-scale disease causality discovery from biomedical literature*

A study on large-scale disease causality discovery from biomedical literature*

The role of IL-6 in dopamine dysregulation underlying anhedonia phenotype in rats

Enteric neuropathy in diabetes: Implications for gastrointestinal function

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