Plasma glucagon in diabetes of haemochromatosis: too low or too high?

Müller, W.; Berger, Michael; Cüppers, H J; Berchtold, Peter; Strohmeyer, G; Renold, Albert E.; Hofstetter, J R; Gonvers, J.-J.

doi:10.1136/gut.20.3.200

Cited by 9 publications

(5 citation statements)

References 24 publications

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“…In concordance with a previous study on a-cell function in IHC [18], concentrations of glucagon did not differ between IHC patients and healthy subjects. A study in diabetic IHC patients has shown that, in this stage of the disease, glucagon hypersecretion can be observed as in other types of diabetes [19].…”

Section: Discussionsupporting

confidence: 92%

Hyperinsulinaemia in non-cirrhotic haemochromatosis: impaired hepatic insulin degradation?

et al. 1984

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This study investigated early alterations of glucose metabolism in idiopathic haemochromatosis. Circulating concentrations of glucose, insulin, C-peptide, glucagon, and gastric inhibitory polypeptide (GIP) were measured after a 100-g oral glucose load in 10 men with idiopathic haemochromatosis in the non-cirrhotic stage of the disease. All had normal glucose tolerance and normal body weight. Ten matched healthy subjects were studied as controls. Insulin concentrations increased to significantly higher levels in patients with idiopathic haemochromatosis than in the control subjects from 30 to 180 min after the glucose load (p less than or equal to 0.01), while fasting insulin concentrations were not significantly different (p greater than 0.05). Concentrations of glucose, glucagon, C-peptide, and GIP were not significantly different at any time (p greater than 0.05). Thus, patients with idiopathic haemochromatosis show hyperinsulinaemia and hence insulin resistance without impaired glucose tolerance in the non-cirrhotic stage. Since pancreatic insulin secretion (C-peptide), glucagon secretion, and the entero-insulinar axis (GIP) are not impaired in these non-cirrhotic patients with idiopathic haemochromatosis, iron accumulation in the hepatocytes may be responsible for the impaired insulin effect and may cause impaired hepatic insulin extraction.

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Section: Discussionsupporting

confidence: 92%

Hyperinsulinaemia in non-cirrhotic haemochromatosis: impaired hepatic insulin degradation?

et al. 1984

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“…The inter‐assay coefficient of variation was 9% between 100 and 350 pg ml −1 , the intra‐assay coefficient of variation was 2.6% at 20 pg ml −1 . In order to assess the possible contribution of big plasma glucagon (BPG) to the total glucagon levels, basal plasma samples were additionally assayed after charcoal treatment, as previously described [9]. The remaining immunoreactive glucagon is predominantly large molecular weight glucagon (MW > 20000).…”

Section: Methodsmentioning

confidence: 99%

Pulsatile insulin infusion and glucose‐homeostasis in well‐controlled Type 1 (insulin‐dependent) diabetic patients

Heinemann

Sonnenberg

Hohmann

et al. 1989

Journal of Internal Medicine

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Pulsatile, intravenous insulin infusion designed to mimic the portal insulin concentrations that emerge physiologically after a meal, has been postulated to improve glucose tolerance in Type 1 (insulin-dependent) diabetic patients. We studied the effects of insulin pulsing (10 i.v. pulses of human insulin of 0.035 U kg-1 idealised body weight were given, each of 20 s duration, with intervals of 6 min, three times per day covered with adequate administration of glucose) on 2 successive days on glucose-tolerance in nine well-controlled Type 1 diabetic patients on continuous subcutaneous insulin infusion therapy (age 26 (7) years, mean (SD); duration of diabetes 10 (7) years; body mass index 23.4 (2.3) kg m-2; HbA1c 6.0 (0.6)%). On the days before and after the insulin pulsing, the patients were subjected to metabolic assessments by an oral glucose tolerance test (1 g glucose kg-1 body weight) 30 min after the subcutaneous injection of 0.15 U kg-1 body weight regular human insulin and a subsequent bicycle-ergometer test. During these metabolic assessments, plasma free insulin concentrations, plasma glucagon and the non-protein respiratory quotient remained unaffected by the insulin pulsing. However, glucose tolerance deteriorated significantly (maximal glucose concentration 120 min after glucose load was 10.0 mmol l-1 before and 13.9 mmol l-1 after insulin pulsing, P less than 0.01). In conclusion, the pattern of insulin pulsing used in this study did not ameliorate oral glucose homeostasis in well-controlled Type 1 (insulin dependent) diabetic patients.

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“…Patients with hemochromatosis and impaired glucose tolerance or diabetes have enhanced glucagon responses after arginine infusion [ 54 – 59 ]. In one study, glucagon immunoreactivity in plasma was higher in patients with hemochromatosis than in control subjects, regardless of glucose tolerance [ 57 ]. When nonspecific reactivity was deducted, the resulting values for true glucagon concentrations were similar in hemochromatosis and control subjects [ 57 ].…”

Section: Diabetes Pathogenesis In Hemochromatosismentioning

confidence: 99%

“…In one study, glucagon immunoreactivity in plasma was higher in patients with hemochromatosis than in control subjects, regardless of glucose tolerance [ 57 ]. When nonspecific reactivity was deducted, the resulting values for true glucagon concentrations were similar in hemochromatosis and control subjects [ 57 ]. It can be inferred from these reports that alpha-cell function is preserved in typical patients with hemochromatosis and diabetes [ 58 ].…”

Section: Diabetes Pathogenesis In Hemochromatosismentioning

confidence: 99%

Diabetes inHFEHemochromatosis

Barton

Acton

2017

Journal of Diabetes Research

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Diabetes in whites of European descent with hemochromatosis was first attributed to pancreatic siderosis. Later observations revealed that the pathogenesis of diabetes in HFE hemochromatosis is multifactorial and its clinical manifestations are heterogeneous. Increased type 2 diabetes risk in HFE hemochromatosis is associated with one or more factors, including abnormal iron homeostasis and iron overload, decreased insulin secretion, cirrhosis, diabetes in first-degree relatives, increased body mass index, insulin resistance, and metabolic syndrome. In p.C282Y homozygotes, serum ferritin, usually elevated at hemochromatosis diagnosis, largely reflects body iron stores but not diabetes risk. In persons with diabetes type 2 without hemochromatosis diagnoses, serum ferritin levels are higher than those of persons without diabetes, but most values are within the reference range. Phlebotomy therapy to achieve iron depletion does not improve diabetes control in all persons with HFE hemochromatosis. The prevalence of type 2 diabetes diagnosed today in whites of European descent with and without HFE hemochromatosis is similar. Routine iron phenotyping or HFE genotyping of patients with type 2 diabetes is not recommended. Herein, we review diabetes in HFE hemochromatosis and the role of iron in diabetes pathogenesis in whites of European descent with and without HFE hemochromatosis.

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Plasma glucagon in diabetes of haemochromatosis: too low or too high?

Cited by 9 publications

References 24 publications

Hyperinsulinaemia in non-cirrhotic haemochromatosis: impaired hepatic insulin degradation?

Hyperinsulinaemia in non-cirrhotic haemochromatosis: impaired hepatic insulin degradation?

Pulsatile insulin infusion and glucose‐homeostasis in well‐controlled Type 1 (insulin‐dependent) diabetic patients

Diabetes inHFEHemochromatosis

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