Normal Glucose Homeostasis

Shrayyef, Muhammad; Gerich, John E.

doi:10.1007/978-0-387-09841-8_2

Cited by 46 publications

(49 citation statements)

References 78 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In contrast, other cells, such as β cells, neuronal, and endothelial cells, are unable to activate this control of glucose afflux and they equilibrate their intracellular glucose level to the extracellular concentrations, and therefore are more susceptible to the effect of hyperglycemia. 1,2,28 In the context of diabetes, hyperglycemia can cause acute and chronic complications, which represent important determinants of morbidity and mortality, and have a negative impact on the prognosis of people affected by this disease. 29 …”

Section: Complications Of Hyperglycemiamentioning

confidence: 99%

Complications of Acute and Chronic Hyperglycemia

Marcovecchio¹

2017

US Endocrinology

View full text Add to dashboard Cite

Hyperglycemia is due to a dysregulation in the complex mechanisms implicated in glucose homeostasis. Chronic hyperglycemia, as measured by hemoglobin A1c (HbA1c), is a key risk factor for the development of microvascular and macrovascular complications, which in turn negatively influence the prognosis of patients with diabetes. Several studies have shown that acute hyperglycemia can add to the effect of chronic hyperglycemia in inducing tissue damage. Acute hyperglycemia can manifest as high fasting plasma glucose (FPG) or high postprandial plasma glucose (PPG) and can activate the same metabolic and hemodynamic pathways as chronic hyperglycemia. Glucose variability, as expressed by the intraday glucose fluctuations from peaks to nadirs, is another important parameter, which has emerged as an HbA1c-independent risk factor for the development of vascular complications, mainly in the context of type 2 diabetes. Treatments able to decrease HbA1c have been associated with positive effects in terms of reducing risk for the development and progression of complications. Further studies are required to clarify the impact of strategies more specifically targeting components of acute hyperglycemia, to improve outcomes in patients with diabetes. KeywordsHyperglycemia, complications, vascular, acute, chronic Disclosure: M Loredana Marcovecchio has nothing to disclose in relation to this article. No funding was received in the publication of this article. This study involves a review of the literature and did not involve any studies with human or animal subjects performed by any of the authors.Authorship: Thel named author meets the International Committee of Medical Journal Editors (ICMJE) criteria for authorship of this manuscript, takes responsibility for the integrity of the work as a whole, and has given final approval to the version to be published.Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit. From glucose homeostasis to hyperglycemiaGlucose homeostasis is maintained by a complex neurohormonal system, which modulates peripheral glucose uptake, hepatic glucose production, and exogenous glucose utilization following food ingestion.1,2 This allows the maintenance of plasma glucose concentrations within normal range, with average values of around 90 mg/dl throughout a 24-hour period, postmeal concentration below 140 mg/dl, and minimal values, such as those after moderate fasting or exercise, above 55 mg/dl. 1,2Hormones implicated in glucose regulation include insulin, glucagon, amylin, glucagon-like petide-1 (GLP-1), glucose-dependent insulinotropic peptide, epinephrine, cortisol, and growth hormone. These hormones act on several target tissues, including muscle, liver, adipocyte, and brain to regulate glucose levels. 3Insulin is a key glucoregulatory hormone, produced by pancreatic β-cells, whose levels are low durin...

show abstract

Section: Complications Of Hyperglycemiamentioning

confidence: 99%

Complications of Acute and Chronic Hyperglycemia

Marcovecchio¹

2017

US Endocrinology

View full text Add to dashboard Cite

show abstract

“…The liver can only produce glucose in two ways: glycogenolysis and gluconeogenesis. In humans, glycogenolysis is initially responsible for most of the glucose produced in the post-absorptive state, but it is progressively replaced by gluconeogenesis as liver glycogen reaches depletion (Shrayyef and Gerich, 2010;Wasserman, 2009). In fish, the relative importance of the two pathways has not been established, and both may contribute to R a glucose under our conditions.…”

Section: Suppression Of Hepatic Glucose Productionmentioning

confidence: 99%

“…Current information shows that insulin plays a major role in blocking R a glucose in animals undergoing acute elevation in glycemia. In mammals as well as trout, hepatic production is decreased when high insulin levels inhibit glucose release in the circulation by terminating the transcription of glucose 6-phosphatase (G6Pase) (Polakof et al, 2010a;Rojas and Schwartz, 2014 mammals (Shrayyef and Gerich, 2010). Similarly, gluconeogenesis is inhibited by high levels of insulin, which inhibits transcription of mammalian phosphoenolpyruvate carboxykinase (PEPCK) (Rojas and Schwartz, 2014).…”

Section: Suppression Of Hepatic Glucose Productionmentioning

confidence: 99%

“…The multiple mechanisms that allow fine regulation of glucose fluxes from hepatic production to muscle uptake and metabolism (insulin, glucagon, glucose transporters and muscle hexokinase) have been well characterized (Shrayyef and Gerich, 2010;Wasserman et al, 2011). Measurements of glucose kinetics in diabetic humans have showed that R a and R d can both be chronically stimulated (Meyer et al, 1998), and the infusion of exogenous glucose has been used to test the limits of mammalian plasticity for glucose fluxes.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Pushing the limits of glucose kinetics: how rainbow trout cope with a carbohydrate overload

Choi

Weber

2015

Journal of Experimental Biology

View full text Add to dashboard Cite

Rainbow trout are generally considered to be poor glucoregulators. To evaluate this, exogenous glucose was administered to chronically hyperglycemic fish at twice the endogenous rate of hepatic production, and their ability to modulate glucose fluxes was tested. Our goals were to determine: (1) whether hyperglycemic fish maintain higher glucose fluxes than normal; (2) whether they can lower hepatic production (R a glucose) or stimulate disposal (R d glucose) to cope with a carbohydrate overload; and (3) an estimate of the relative importance of glucose as an oxidative fuel. Results show that hyperglycemic trout sustain elevated baseline R a and R d glucose of 10.6±0.1 µmol kg −1 min −1 (or 30% above normal). If 50% of R d glucose was oxidized as in mammals, glucose could account for 36 to 100% of metabolic rate when exogenous glucose is supplied. In response to exogenous glucose, rainbow trout can completely suppress hepatic glucose production and increase disposal 2.6-fold, even with chronically elevated baseline fluxes. Such large changes in fluxes limit the increase in blood glucose to 2.5-fold and are probably mediated by the effects of insulin on glucose transporters 2 and 4 and on key enzymes of carbohydrate metabolism. Without this strong and rapid modulation of glucose kinetics, glycemia would rise four times faster to reach dangerous levels, exceeding 100 mmol l −1. Such responses are typical of mammals, but rather unexpected for an ectotherm. The impressive plasticity of glucose kinetics demonstrated here suggests that trout have a much better glucoregulatory capacity than is usually portrayed in the literature.

show abstract

“…About half of this glucose comes from the breakdown of stored glycogen, and the rest from the metabolism of sources other than carbohydrate or glycogen, including certain amino acids, through a process known as gluconeogenesis. 8 Interactions between muscle and liver are largely responsible for regulating carbohydrate metabolism and for achieving energy balance in normal fed and fasted states; the kidneys play a role similar to that of the liver, but to a lesser extent. 3,8 In addition, muscle tissue stores amino acids as protein, and adipose tissue serves as a depot of glycerol and fatty acids.…”

Section: Muscle Metabolism and Interorgan Crosstalkmentioning

confidence: 99%

Skeletal Muscle Regulates Metabolism via Interorgan Crosstalk: Roles in Health and Disease

Argilés

Campos

López-Pedrosa

et al. 2016

Journal of the American Medical Directors Association

375

270

View full text Add to dashboard Cite

Skeletal muscle is recognized as vital to physical movement, posture, and breathing. In a less known but critically important role, muscle influences energy and protein metabolism throughout the body. Muscle is a primary site for glucose uptake and storage, and it is also a reservoir of amino acids stored as protein. Amino acids are released when supplies are needed elsewhere in the body. These conditions occur with acute and chronic diseases, which decrease dietary intake while increasing metabolic needs. Such metabolic shifts lead to the muscle loss associated with sarcopenia and cachexia, resulting in a variety of adverse health and economic consequences. With loss of skeletal muscle, protein and energy availability is lowered throughout the body. Muscle loss is associated with delayed recovery from illness, slowed wound healing, reduced resting metabolic rate, physical disability, poorer quality of life, and higher health care costs. These adverse effects can be combatted with exercise and nutrition. Studies suggest dietary protein and leucine or its metabolite β-hydroxy β-methylbutyrate (HMB) can improve muscle function, in turn improving functional performance. Considerable evidence shows that use of high-protein oral nutritional supplements (ONS) can help maintain and rebuild muscle mass and strength. We review muscle structure, function, and role in energy and protein balance. We discuss how disease- and age-related malnutrition hamper muscle accretion, ultimately causing whole-body deterioration. Finally, we describe how specialized nutrition and exercise can restore muscle mass, strength, and function, and ultimately reverse the negative health and economic outcomes associated with muscle loss.

show abstract

Normal Glucose Homeostasis

Cited by 46 publications

References 78 publications

Complications of Acute and Chronic Hyperglycemia

Complications of Acute and Chronic Hyperglycemia

Pushing the limits of glucose kinetics: how rainbow trout cope with a carbohydrate overload

Skeletal Muscle Regulates Metabolism via Interorgan Crosstalk: Roles in Health and Disease

Contact Info

Product

Resources

About