The Physiology of Glucagon

Taborsky, Gerald J.

doi:10.1177/193229681000400607

Cited by 78 publications

(63 citation statements)

References 88 publications

(101 reference statements)

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“…Plasma glucose is derived from the feed, glycogen, and by gluconeogenesis, and it is regulated by several hormones, mainly glucagon and insulin. Glucagon increases plasma glucose concentration through stimulation of gluconeogenesis and glycogenolysis (Aronoff et al, 2004;Taborsky, 2010). Changes in glucagon secretion from the physiological range results in changes of plasma glucose concentration (Taborsky, 2010); some substrates, such as NEFA and ketone bodies, suppress glucagon secretion (Gerich et al, 1974;1976;Goberna et al, 1974).…”

Section: Discussionmentioning

confidence: 99%

“…Glucagon increases plasma glucose concentration through stimulation of gluconeogenesis and glycogenolysis (Aronoff et al, 2004;Taborsky, 2010). Changes in glucagon secretion from the physiological range results in changes of plasma glucose concentration (Taborsky, 2010); some substrates, such as NEFA and ketone bodies, suppress glucagon secretion (Gerich et al, 1974;1976;Goberna et al, 1974). Evidence exists that glucagon secretion is inhibited by the neighboring beta cell through insulin (Weir et al, 1976) and γ-aminobutyric acid (GABA; Adeghate et al, 2000;Wendt et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

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Long-term elevation of β-hydroxybutyrate in dairy cows through infusion: Effects on feed intake, milk production, and metabolism

Zarrin

Matteis

Vernay

et al. 2013

Journal of Dairy Science

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Elevation of ketone bodies in dairy cows frequently occurs in early lactation, usually concomitantly with a lack of energy and glucose. The objective of this study was to induce an elevated plasma β-hydroxybutyrate (BHBA) concentration over 48 h in mid-lactating dairy cows (i.e., during a period of positive energy balance and normal glucose plasma concentrations). Effects of BHBA infusion on feed intake, metabolism, and performance were investigated. Thirteen cows were randomly assigned to 1 of 2 infusion groups, including an intravenous infusion with Na-dl-β-OH-butyrate (1.7 mol/L) to achieve a plasma concentration of 1.5 to 2.0 mmol/L of BHBA (HyperB; n = 5), or an infusion of 0.9% saline solution (control; n = 8). Blood was sampled before and hourly during the 48 h of infusion. In the liver, mRNA transcripts related to gluconeogenesis (pyruvate carboxylase, glucose 6-phosphatase, mitochondrial phosphoenolpyruvate carboxykinase), phosphofructokinase, pyruvate dehydrogenase complex, and fatty acid synthesis (acetyl-coenzyme A carboxylase, fatty acid synthase) were measured by real-time PCR. Glyceraldehyde-3-phosphate dehydrogenase and ubiquitin were used as housekeeping genes. Changes (difference between before and after 48-h infusion) during the infusion period were evaluated by ANOVA with treatment as fixed effect, and area under the curve of variables was calculated on the second day of experiment. The plasma BHBA concentration in HyperB cows was 1.74 ± 0.02 mmol/L (mean ± SE) compared with 0.59 ± 0.02 mmol/L for control cows. The change in feed intake, milk yield, and energy corrected milk did not differ between the 2 experimental groups. Infusion of BHBA reduced the plasma glucose concentration (3.47 ± 0.11 mmol/L) in HyperB compared with control cows (4.11 ± 0.08 mmol/L). Plasma glucagon concentration in HyperB was lower than the control group. All other variables measured in plasma were not affected by treatment. In the liver, changes in mRNA abundance for the selected genes were similar between 2 groups. Results demonstrate that intravenous infusion of BHBA decreased plasma glucose concentration in dairy cows, but this decrease could not be explained by alterations in insulin concentrations or key enzymes related to gluconeogenesis. Declined glucose concentration is likely functionally related to decreased plasma glucagon concentration.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Long-term elevation of β-hydroxybutyrate in dairy cows through infusion: Effects on feed intake, milk production, and metabolism

Zarrin

Matteis

Vernay

et al. 2013

Journal of Dairy Science

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“…2 Glucagon is secreted from alpha pancreatic cells into the portal vein and promotes hepatic glucose production during fasting via glucogenolysis and gluconeogenesis. 2,8 After food consumption glucagon secretion is suppressed by insulin, amylin and GLP1. Glucagon plays a significant role in postprandial hyperglycemia.…”

Section: (Figure 1)mentioning

confidence: 99%

Postprandial dysmetabolism: Too early or too late?

Pappas¹,

Kandaraki²,

Tsirona³

et al. 2016

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postprandial dysmetabolism is a postprandial state characterized by abnormal metabolism of glucose and lipids and, more specifically, of elevated levels of glucose and triglyceride (Tg) containing lipoproteins. Since there is evidence that postprandial dysmetabolism is associated with increased cardiovascular mortality and morbidity, due to macro-and microvascular complications, as well as with conditions such as polycystic ovary syndrome (pCOS) and nonalcoholic fatty liver disease (NaFlD), it is recommended that clinicians be alert for early detection and management of this condition. management consists of a holistic approach including dietary modification, exercise and use of hypoglycemic and hypolipidemic medication aiming to decrease the postprandial values of circulating glucose and triglycerides. This review aims to explain glucose and lipid homeostasis and the impact of postprandial dysmetabolism on the cardiovascular system as well as to offer suggestions with regard to the therapeutic approach for this entity. however, more trials are required to prevent or reverse early and not too late the actual tissue damage due to postprandial dysmetabolism.

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“…The islets of Langerhans are innervated by the sympathetic nervous system [1,16]. Secretion of insulin by cells in these islets is inhibited by the neurotransmitter noradrenaline (NA) through activation of α2-adrenergic receptors coupled to G proteins [1,19].…”

Section: Introductionmentioning

confidence: 99%

Sympathetic Voltage-Independent Regulation of Voltage- Gated Calcium Channels in Pancreatic β-Cells

Cruz¹,

Reyes-Vaca²,

Garduño³

et al. 2018

JED

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Voltage-gated calcium (Ca V ) channels are regulated by G proteins via voltage-dependent and independent pathways. Voltage-independent regulation of calcium channels is important for intracellular calcium concentration and insulin secretion. Voltage dependence of each pathway can be elucidated by a prepulse facilitation protocol. Using this experimental approach, we compared Ca V regulation by GTPγS and noradrenaline (NA) in rat pancreatic β-cells and rat superior cervical ganglion (SCG) neurons. The SCG neuron is a model in which the bases of Ca V channel regulation by G proteins have been established. Ca V channel regulation through activation of the sympathetic nervous system has been poorly studied in native insulin-secreting cells. We recorded Ca V channel currents by means of the patch-clamp technique in the whole-cell configuration. We found that application of both GTPγS (a nonspecific activator of G proteins) by cell dialysis and noradrenaline (NA)-exposure reduced Ca V current amplitude in pancreatic β-cells and in SCG neurons. However, the inhibition of Ca V channel currents in GTPγS-dialyzed SCG neurons was relieved by a strong depolarizing pulse. By contrast, in pancreatic β-cells, the inhibition was maintained after a strong depolarizing pulse. In SCG neurons, the Ca V channel inhibition by NA is predominantly voltage-dependent, whereas in pancreatic β-cells it is only 40%. Thus, it appears that Ca V channels in rat pancreatic β-cells are regulated mainly through a voltage-independent pathway. The signaling pathway for Ca V channel regulation by NA in pancreatic β-cells appears to differ from the classic signaling pathway described in SCG neurons. Therefore, voltage-independent regulation of Ca 2+ entry through Ca V channels is a critical step in understanding the pathophysiology of type 2 diabetes.

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The Physiology of Glucagon

Cited by 78 publications

References 88 publications

Long-term elevation of β-hydroxybutyrate in dairy cows through infusion: Effects on feed intake, milk production, and metabolism

Long-term elevation of β-hydroxybutyrate in dairy cows through infusion: Effects on feed intake, milk production, and metabolism

Postprandial dysmetabolism: Too early or too late?

Sympathetic Voltage-Independent Regulation of Voltage- Gated Calcium Channels in Pancreatic β-Cells

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