Type 2 Diabetes Mellitus (T2DM) and Carbohydrate Metabolism in Relation to T2DM from Endocrinology, Neurophysiology, Molecular Biology, and Biochemistry Perspectives

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Abstract

Type 2 diabetes mellitus (T2DM) is a severe disease caused by metabolic disorders, particularly carbohydrate metabolism disorders. The disease is a fatal global trouble characterised by high prevalence rates, causing death, blindness, kidney failure, myocardial infarction, amputation of lower limps, and stroke. Biochemical metabolic pathways like glycolysis, gluconeogenesis, glycogenesis, and glycogenolysis are critical pathways that regulate blood glucose levels with the glucokinase (GK) enzyme playing a central role in glucose homeostasis. Any factor that perturbs the aforementioned biochemical pathways is detrimental. Endocrinological, neurophysiological, and molecular biological pathways that are linked to carbohydrate metabolism should be studied, grasped, and manipulated in order to alleviate T2DM global chaos. The challenge, howbeit, is that, since the body is an integration of systems that complement one another, studying one “isolated” system is not very useful. This paper serves to discuss endocrinology, neurophysiology, and molecular biology pathways that are involved in carbohydrate metabolism in relation to T2DM.

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The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation

Nathan Kelley, Devon Jeltema, Yanhui Duan … (2019)

The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage. However, the aberrant activation of the NLRP3 inflammasome has been linked with several inflammatory disorders, which include cryopyrin-associated periodic syndromes, Alzheimer’s disease, diabetes, and atherosclerosis. The NLRP3 inflammasome is activated by diverse stimuli, and multiple molecular and cellular events, including ionic flux, mitochondrial dysfunction, and the production of reactive oxygen species, and lysosomal damage have been shown to trigger its activation. How NLRP3 responds to those signaling events and initiates the assembly of the NLRP3 inflammasome is not fully understood. In this review, we summarize our current understanding of the mechanisms of NLRP3 inflammasome activation by multiple signaling events, and its regulation by post-translational modifications and interacting partners of NLRP3.

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The NALP3/NLRP3 Inflammasome Instigates Obesity-Induced Autoinflammation and Insulin Resistance

Bolormaa Vandanmagsar, Yun-Hee Youm, Anthony Ravussin … (2011)

Emergence of chronic ‘sterile’ inflammation during obesity in absence of overt infection or autoimmune process is a puzzling phenomenon. The Nod Like Receptor (NLR) family of innate immune cell sensors like the Nlrp3 inflammasome are implicated in recognizing certain non-microbial origin ‘danger–signals’ leading to caspase-1 activation and subsequent IL-1β and IL-18 secretion. We show that reduction in adipose tissue expression of Nlrp3 is coupled with decreased inflammation and improved insulin–sensitivity in obese type-2 diabetic patients. The Nlrp3 inflammasome senses the lipotoxicity–associated ceramide to induce caspase-1 cleavage in macrophages and adipose tissue. Ablation of Nlrp3 prevented the obesity–induced inflammasome activation in fat depots and liver together with enhanced insulin–signalling. Furthermore, elimination of Nlrp3 in obesity reduced IL-18 and adipose tissue IFNγ along with an increase in naïve and reduction in effector adipose tissue T cells. Collectively, these data establish that Nlrp3 inflammasome senses obesity–associated ‘danger–signals’ and contributes to obesity–induced inflammation and insulin–resistance.

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Prevalence and control of diabetes in Chinese adults.

Yu Xu, Limin Wang, Jiang Ping He … (2013)

Noncommunicable chronic diseases have become the leading causes of mortality and disease burden worldwide. To investigate the prevalence of diabetes and glycemic control in the Chinese adult population. Using a complex, multistage, probability sampling design, we conducted a cross-sectional survey in a nationally representative sample of 98,658 Chinese adults in 2010. Plasma glucose and hemoglobin A1c levels were measured after at least a 10-hour overnight fast among all study participants, and a 2-hour oral glucose tolerance test was conducted among participants without a self-reported history of diagnosed diabetes. Diabetes and prediabetes were defined according to the 2010 American Diabetes Association criteria; whereas, a hemoglobin A1c level of <7.0% was considered adequate glycemic control. The overall prevalence of diabetes was estimated to be 11.6% (95% CI, 11.3%-11.8%) in the Chinese adult population. The prevalence among men was 12.1% (95% CI, 11.7%-12.5%) and among women was 11.0% (95% CI, 10.7%-11.4%). The prevalence of previously diagnosed diabetes was estimated to be 3.5% (95% CI, 3.4%-3.6%) in the Chinese population: 3.6% (95% CI, 3.4%-3.8%) in men and 3.4% (95% CI, 3.2%-3.5%) in women. The prevalence of undiagnosed diabetes was 8.1% (95% CI, 7.9%-8.3%) in the Chinese population: 8.5% (95% CI, 8.2%-8.8%) in men and 7.7% (95% CI, 7.4%-8.0%) in women. In addition, the prevalence of prediabetes was estimated to be 50.1% (95% CI, 49.7%-50.6%) in Chinese adults: 52.1% (95% CI, 51.5%-52.7%) in men and 48.1% (95% CI, 47.6%-48.7%) in women. The prevalence of diabetes was higher in older age groups, in urban residents, and in persons living in economically developed regions. Among patients with diabetes, only 25.8% (95% CI, 24.9%-26.8%) received treatment for diabetes, and only 39.7% (95% CI, 37.6%-41.8%) of those treated had adequate glycemic control. The estimated prevalence of diabetes among a representative sample of Chinese adults was 11.6% and the prevalence of prediabetes was 50.1%. Projections based on sample weighting suggest this may represent up to 113.9 million Chinese adults with diabetes and 493.4 million with prediabetes. These findings indicate the importance of diabetes as a public health problem in China.

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Author and article information

Contributors

Hilla Mills:

ORCID: https://orcid.org/0000-0003-2032-9279

Luke Cheung:

ORCID: https://orcid.org/0000-0003-2723-5910

Ronald Glassen:

ORCID: https://orcid.org/0000-0003-3195-5718

Alain Albert:

ORCID: https://orcid.org/0000-0003-1012-7331

Thang Nguyen Van:

ORCID: https://orcid.org/0000-0003-1628-0011

Journal

Journal ID (nlm-ta): Evid Based Complement Alternat Med

Journal ID (iso-abbrev): Evid Based Complement Alternat Med

Journal ID (publisher-id): ECAM

Title: Evidence-based Complementary and Alternative Medicine : eCAM

Publisher: Hindawi

ISSN (Print): 1741-427X

ISSN (Electronic): 1741-4288

Publication date Collection: 2022

Publication date (Electronic): 9 August 2022

Publication date PMC-release: 9 August 2022

Volume: 2022

Electronic Location Identifier: 1708769

Affiliations

¹Department of Medical Science, University for Development, Accra, Ghana

²RD Lab, The Hospital Institute for Hebal Research, Toluca 50200, MEX, Mexico

³Research Institution of Clinical Biomedicine, Hospital University Medical Centre, Ulm 89000, Germany

⁴Industrial Research Group, International College of Science and Technology, Route de Lennik 800, CP 590, Brussels 1070, Belgium

⁵Clinical Analysis Lab, Center of Bio-Medicine, Hanoi, Vietnam

Author notes

Academic Editor: Weiguo Li

Author information

Hilla Mills https://orcid.org/0000-0003-2032-9279

Ronald Acquah https://orcid.org/0000-0002-5375-6106

Nova Tang https://orcid.org/0000-0002-5745-3663

Luke Cheung https://orcid.org/0000-0003-2723-5910

Susanne Klenk https://orcid.org/0000-0002-4971-5192

Ronald Glassen https://orcid.org/0000-0003-3195-5718

Magali Pirson https://orcid.org/0000-0001-8468-3184

Alain Albert https://orcid.org/0000-0003-1012-7331

Duong Trinh Hoang https://orcid.org/0000-0002-4463-4270

Thang Nguyen Van https://orcid.org/0000-0003-1628-0011

Article

DOI: 10.1155/2022/1708769

PMC ID: 9381199

PubMed ID: 35983003

SO-VID: f5050616-bbf9-44dc-af89-2789a858608a

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 11 July 2022

Date revision received : 15 July 2022

Date accepted : 18 July 2022

Funding

Funded by: Hospital University Medical Centre

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Type 2 Diabetes Mellitus (T2DM) and Carbohydrate Metabolism in Relation to T2DM from Endocrinology, Neurophysiology, Molecular Biology, and Biochemistry Perspectives

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The International Journal of Person Centered Medicine

Most cited references 68

The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation

The NALP3/NLRP3 Inflammasome Instigates Obesity-Induced Autoinflammation and Insulin Resistance

Prevalence and control of diabetes in Chinese adults.

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Cited by 4

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