Antecedent hypoglycemia does not alter increased epinephrine-induced lipolysis in type 1 diabetes mellitus

Hoffman, Robert R.

doi:10.1016/j.metabol.2005.09.012

Cited by 8 publications

(8 citation statements)

References 38 publications

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“…Free fatty acids have also been shown to alter cell membrane glucose transport [60]. Furthermore, during epinephrine infusion and hyperinsulinemic glucose clamp glucose infusion rates negatively correlate with free fatty acid levels in healthy and type 1 diabetic subjects [65]. Glucose infusion rates during insulin clamps are inversely related to fat oxidation rates [62,63] and forearm glucose extraction during hypoglycemia is negatively correlated with arterial free fatty acid levels [64].…”

Section: Glucose Utilizationmentioning

confidence: 99%

“…Some of the differences between studies may be explained by differences in insulin infusion rates with greater infusion rates in type 1 diabetic subjects suppressing lipolysis and potentially masking differences [131,136]. The increased free fatty acid levels during epinephrine infusion in patients with type 1 diabetes are accompanied by decreased muscle glucose utilization suggesting that increased lipolysis directly inhibits muscle glucose uptake [65]. The increased free fatty acid levels during epinephrine infusion in patients with type 1 diabetes are accompanied by decreased muscle glucose utilization suggesting that increased lipolysis directly inhibits muscle glucose uptake [65].…”

Section: Adrenergic Sensitivity In Diabetesmentioning

confidence: 99%

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Sympathetic Mechanisms of Hypoglycemic Counterregulation

Hoffman

2007

CDR

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In normal individuals hypoglycemic counterregulation is a multifactorial, redundant process that involves reduction of insulin secretion, increasing glucagon secretion, adrenergic activation, and increased growth hormone and cortisol secretion. Metabolically, these lead to increased glucose production, initially through glycogenolysis and later through gluconeogenesis, decreased muscle glucose oxidation and storage and increased release and use of alternative fuels, primarily free fatty acids. They also lead to hypoglycemic symptoms and hunger which increase food intake. These systems are designed to provide as much glucose as possible for brain glucose use. In patients with type 1 diabetes there are multiple impairments of these responses. Insulin does not decrease. Glucagon secretion is decreased or absent. Recovery from hypoglycemia is therefore dependent on the adrenergic response. Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both alpha and beta adrenergic activity increase. Increased beta-activity increases free fatty acid release which increase glucose production and decrease glucose utilization. The increased alpha-adrenergic activity's primary role is to counteract beta-adrenergic vasodilation. It may also reduce neurogenic and neuroglycopenic symptoms. Lastly, there is evidence that both cardiac and adrenergic sensitivity are altered in type 1 diabetes. It is hoped that this information can be used in the future to help develop ways to protect patients with type 1 diabetes from hypoglycemia and its adverse effects.

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Section: Glucose Utilizationmentioning

confidence: 99%

Section: Adrenergic Sensitivity In Diabetesmentioning

confidence: 99%

Sympathetic Mechanisms of Hypoglycemic Counterregulation

Hoffman

2007

CDR

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“…Hypoglycemia also seems to impact the physiological response of epinephrine, reducing the cardiovascular, hepatic, and adipose tissue responses to epinephrine 37. Another study, however, did not see the same changes 38. All mentioned studies did not investigate the changes in different metabolites as we did; however, due to the limitation of our study, which did not specifically focus on metabolic responses to epinephrine, further studies looking at the amino acid and lipid fluxes are needed to elaborate our findings.…”

Section: Discussionmentioning

confidence: 95%

Decreased branched-chain amino acids and elevated fatty acids during antecedent hypoglycemia in type 1 diabetes

She

Al-Sari

Mattila

et al. 2023

BMJ Open Diab Res Care

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IntroductionHypoglycemia is a major limiting factor in achieving recommended glycemic targets for people with type 1 diabetes. Exposure to recurrent hypoglycemia results in blunted hormonal counter-regulatory and symptomatic responses to hypoglycemia. Limited data on metabolic adaptation to recurrent hypoglycemia are available. This study examined the acute metabolic responses to hypoglycemia and the effect of antecedent hypoglycemia on these responses in type 1 diabetes.Research design and methodsTwenty-one outpatients with type 1 diabetes with normal or impaired awareness of hypoglycemia participated in a study assessing the response to hypoglycemia on 2 consecutive days by a hyperinsulinemic glucose clamp. Participants underwent a period of normoglycemia and a period of hypoglycemia during the hyperinsulinemic glucose clamp. Plasma samples were taken during normoglycemia and at the beginning and the end of the hypoglycemic period. Metabolomic analysis of the plasma samples was conducted using comprehensive two-dimensional gas chromatography with time-of-flight mass spectrometry.ResultsIn total, 68 metabolites were studied. On day 1, concentrations of the branched-chain amino acids, leucine (p=3.8×10−3) and isoleucine (p=2.2×10−3), decreased during hypoglycemia. On day 2, during hypoglycemia, five amino acids (including leucine and isoleucine) significantly decreased, and two fatty acids (tetradecanoic and oleic acids) significantly increased (p<0.05). Although more metabolites responded to hypoglycemia on day 2, the responses of the single metabolites were not statistically significant between the 2 days.ConclusionsIn individuals with type 1 diabetes, one episode of hypoglycemia decreases leucine and isoleucine concentrations. Antecedent hypoglycemia results in the decrement of five amino acids and increases the concentrations of two fatty acids, suggesting an alteration between the two hypoglycemic episodes, which could indicate a possible adaptation. However, more studies are needed to gain a comprehensive understanding of the consequences of these alterations.Trial registration numberNCT01337362.

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“…When plasma glucose levels decrease below ∼ 80 mg/dL (4.4 mmol/L) [12] , insulin levels begin to decline. Once plasma glucose levels drop below ∼68 mg/dL (3.8 mmol/L), glucagon and epinephrine levels increase, with the former playing the primary role and the latter a secondary role [6] , [13] , [14] , [15] . Growth hormone (GH) levels rise when glucose is ∼ 67 mg/dL and cortisol when glucose is ∼ 55 mg/dL (3.1 mmol/L), however they likely do not play a critical role in acutely restoring euglycemia since their effects are more protracted over several hours [1] , [6] , [16] .…”

Section: Normal Physiologic Counterregulatory Response To Hypoglycemia and Alterations In Diabetesmentioning

confidence: 99%

Spontaneous and iatrogenic hypoglycemia in cystic fibrosis

Hicks

Marks

Oxman³

et al. 2021

Journal of Clinical & Translational Endocrinology

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Highlights Spontaneous fasting and/or postprandial hypoglycemia is common in people with CF. The clinical significance of OGTT related hypoglycemia in CF is not clear. Dietary modification is the first line treatment for postprandial hypoglycemia. Patients with CFRD are at risk of hypoglycemia related to insulin therapy. CGMs and closed loop insulin pump systems may reduce hypoglycemia risk in CFRD.

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Antecedent hypoglycemia does not alter increased epinephrine-induced lipolysis in type 1 diabetes mellitus

Cited by 8 publications

References 38 publications

Sympathetic Mechanisms of Hypoglycemic Counterregulation

Sympathetic Mechanisms of Hypoglycemic Counterregulation

Decreased branched-chain amino acids and elevated fatty acids during antecedent hypoglycemia in type 1 diabetes

Spontaneous and iatrogenic hypoglycemia in cystic fibrosis

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