Exploring the Mediators that Promote Carotid Body Dysfunction in Type 2 Diabetes and Obesity Related Syndromes

Carotid bodies (CBs) are peripheral chemoreceptors that sense changes in blood O2, CO2, and pH levels. Apart from ventilatory control, these organs are deeply involved in the homeostatic regulation of carbohydrates and lipid metabolism and inflammation. It has been described that CB dysfunction is involved in the genesis of metabolic diseases and that CB overactivation is present in animal models of metabolic disease and in prediabetes patients. Additionally, resection of the CB-sensitive nerve, the carotid sinus nerve (CSN), or CB ablation in animals prevents and reverses diet-induced insulin resistance and glucose intolerance as well as sympathoadrenal overactivity, meaning that the beneficial effects of decreasing CB activity on glucose homeostasis are modulated by target-related efferent sympathetic nerves, through a reflex initiated in the CBs. In agreement with our pre-clinical data, hyperbaric oxygen therapy, which reduces CB activity, improves glucose homeostasis in type 2 diabetes patients. Insulin, leptin, and pro-inflammatory cytokines activate the CB. In this manuscript, we review in a concise manner the putative pathways linking CB chemoreceptor deregulation with the pathogenesis of metabolic diseases and discuss and present new data that highlight the roles of hyperinsulinemia, hyperleptinemia, and chronic inflammation as major factors contributing to CB dysfunction in metabolic disorders.

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Hyperbaric Oxygen Therapy Improves Glucose Homeostasis in Type 2 Diabetes Patients: A Likely Involvement of the Carotid Bodies

Advances in Experimental Medicine and Biology - Arterial Chemoreceptors in Physiology and Pathophysiology ◽

10.1007/978-3-319-18440-1_24 ◽

2015 ◽

pp. 221-225 ◽

Cited By ~ 14

Author(s):

P. Vera-Cruz ◽

F. Guerreiro ◽

M. J. Ribeiro ◽

M. P. Guarino ◽

S. V. Conde

Keyword(s):

Type 2 Diabetes ◽

Hyperbaric Oxygen ◽

Glucose Homeostasis ◽

Hyperbaric Oxygen Therapy ◽

Oxygen Therapy ◽

Carotid Bodies ◽

Diabetes Patients

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Health beneficial effects of resistant starch on diabetes and obesity via regulation of gut microbiota: a review

Food & Function ◽

10.1039/d0fo00855a ◽

2020 ◽

Vol 11 (7) ◽

pp. 5749-5767

Author(s):

Huicui Liu ◽

Min Zhang ◽

Qingyu Ma ◽

Baoming Tian ◽

Chenxi Nie ◽

...

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Gut Microbiota ◽

Resistant Starch ◽

Beneficial Effects ◽

Diabetes And Obesity

Resistant starch (RS) is well known to prevent type 2 diabetes mellitus (T2DM) and obesity.

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Effects of Artificial Sweetener Consumption on Glucose Homeostasis and Its Association with Type 2 Diabetes and Obesity

International Journal of General Medicine ◽

10.2147/ijgm.s274760 ◽

2020 ◽

Vol Volume 13 ◽

pp. 775-785

Author(s):

Ahmed Abdulrahman Alsunni

Keyword(s):

Type 2 Diabetes ◽

Glucose Homeostasis ◽

Artificial Sweetener ◽

Diabetes And Obesity

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Astrocyte Clocks and Glucose Homeostasis

Frontiers in Endocrinology ◽

10.3389/fendo.2021.662017 ◽

2021 ◽

Vol 12 ◽

Author(s):

Olga Barca-Mayo ◽

Miguel López

Keyword(s):

Type 2 Diabetes ◽

Insulin Sensitivity ◽

Glucose Metabolism ◽

Circadian Clock ◽

Glucose Homeostasis ◽

Metabolic Diseases ◽

Current Knowledge ◽

Genetic Alterations ◽

Whole Body

The endogenous timekeeping system evolved to anticipate the time of the day through the 24 hours cycle of the Earth’s rotation. In mammals, the circadian clock governs rhythmic physiological and behavioral processes, including the daily oscillation in glucose metabolism, food intake, energy expenditure, and whole-body insulin sensitivity. The results from a series of studies have demonstrated that environmental or genetic alterations of the circadian cycle in humans and rodents are strongly associated with metabolic diseases such as obesity and type 2 diabetes. Emerging evidence suggests that astrocyte clocks have a crucial role in regulating molecular, physiological, and behavioral circadian rhythms such as glucose metabolism and insulin sensitivity. Given the concurrent high prevalence of type 2 diabetes and circadian disruption, understanding the mechanisms underlying glucose homeostasis regulation by the circadian clock and its dysregulation may improve glycemic control. In this review, we summarize the current knowledge on the tight interconnection between the timekeeping system, glucose homeostasis, and insulin sensitivity. We focus specifically on the involvement of astrocyte clocks, at the organism, cellular, and molecular levels, in the regulation of glucose metabolism.

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Antioxidant supplemention in the treatment of skeletal muscle insulin resistance: potential mechanisms and clinical relevance

Applied Physiology Nutrition and Metabolism ◽

10.1139/h07-155 ◽

2008 ◽

Vol 33 (1) ◽

pp. 21-31 ◽

Cited By ~ 14

Author(s):

David Wright ◽

Lindsey Sutherland

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Skeletal Muscle ◽

Glucose Homeostasis ◽

Whole Body ◽

Antioxidant Compounds ◽

Muscle Insulin Resistance ◽

Beneficial Effects ◽

Skeletal Muscle Insulin Resistance

The incidence of type 2 diabetes has increased dramatically over the past several decades and this trend is projected to continue into the foreseeable future. Skeletal muscle insulin resistance is thought to be a key development in the pathogenesis of type 2 diabetes. Given this fact, interventions that prevent or reverse impairments in skeletal muscle action can have profound effects on whole-body glucose homeostasis. Traditional approaches used in this regard include exercise, weight loss, and insulin-sensitizing drugs such as thiazolidinediones (TZDs). Although these interventions have proven effective in improving glucose homeostasis, there are adherence issues seen with lifestyle interventions and undesirable side effects have been reported with TZDs. With these points in mind, the development of alternative strategies to maintain or improve skeletal muscle insulin sensitivity is warranted. In this context, the purpose of the present review is to highlight the role of antioxidant compounds in the prevention and treatment of skeletal muscle insulin resistance. Specifically, we will briefly describe the mechanisms of insulin-stimulated skeletal muscle glucose uptake and the potential mediators of oxidative stress induced insulin resistance, highlight data suggesting that antioxidant compounds can have beneficial effects on skeletal muscle insulin action, and discuss potential mechanisms mediating this effect.

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Role of GALNT2 on Insulin Sensitivity, Lipid Metabolism and Fat Homeostasis

International Journal of Molecular Sciences ◽

10.3390/ijms23020929 ◽

2022 ◽

Vol 23 (2) ◽

pp. 929

Author(s):

Alessandra Antonucci ◽

Antonella Marucci ◽

Vincenzo Trischitta ◽

Rosa Di Paola

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Common Ground ◽

Metabolic Diseases ◽

Atherogenic Dyslipidemia ◽

Physiological Processes ◽

Protein Functions ◽

Heavy Burden ◽

Diabetes And Obesity

O-linked glycosylation, the greatest form of post-translational modifications, plays a key role in regulating the majority of physiological processes. It is, therefore, not surprising that abnormal O-linked glycosylation has been related to several human diseases. Recently, GALNT2, which encodes the GalNAc-transferase 2 involved in the first step of O-linked glycosylation, has attracted great attention as a possible player in many highly prevalent human metabolic diseases, including atherogenic dyslipidemia, type 2 diabetes and obesity, all clustered on the common ground of insulin resistance. Data available both in human and animal models point to GALNT2 as a molecule that shapes the risk of the aforementioned abnormalities affecting diverse protein functions, which eventually cause clinically distinct phenotypes (a typical example of pleiotropism). Pathways linking GALNT2 to dyslipidemia and insulin resistance have been partly identified, while those for type 2 diabetes and obesity are yet to be understood. Here, we will provide a brief overview on the present knowledge on GALNT2 function and dysfunction and propose novel insights on the complex pathogenesis of the aforementioned metabolic diseases, which all impose a heavy burden for patients, their families and the entire society.

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