Recovery of Pancreatic β-cell Function in Hemochromatosis: Combined Treatment With Recombinant Human Erythropoietin and Phlebotomy

Inoue, Yasushi; Nakanishi, Kōji; Hiraga, Takaki; Okubo, Minoru; Kosáka, Kinori; Miyakoshi, Shigesaburo; MUTOH, YOSHIMOTO; Kobayashi, Tetsuro

doi:10.1097/00000441-199712000-00008

Cited by 15 publications

(8 citation statements)

References 5 publications

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“…Thus far, two prospective studies using the sTfR:ferritin ratio as a marker of body iron stores found similar significant associations [9,10]. Use of phlebotomy or iron-chelation therapy to reduce ferritin levels was associated with improved glucose tolerance in patients with HH [44,45], healthy blood donors [46], patients with metabolic syndrome [47], and patients with T2DM [48]. These studies support our findings of a significant association between increased body iron stores and T2DM risk.…”

Section: Discussionmentioning

confidence: 95%

Dietary iron intake, body iron stores, and the risk of type 2 diabetes: a systematic review and meta-analysis

Bao

Rong

et al. 2012

BMC Med

232

180

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BackgroundExcess iron has been shown to induce diabetes in animal models. However, the results from human epidemiologic studies linking body iron stores and iron intake to the risk of type 2 diabetes mellitus (T2DM) are conflicting. In this study, we aimed to systematically evaluate the available evidence for associations between iron intake, body iron stores, and the risk of T2DM.MethodsA systematic search of the PubMed/MEDLINE and EMBASE databases to the end of 22 April 2012 was performed, and reference lists of retrieved articles were screened. Two reviewers independently evaluated the eligibility of inclusion and extracted the data. Pooled relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random-effects models.ResultsWe reviewed 449 potentially relevant articles, and 11 prospective studies were included in the analysis. A meta-analysis of five studies gave a pooled RR for T2DM of 1.33 (95% CI 1.19 to 1.48; P<0.001) in individuals with the highest level of heme iron intake, compared with those with the lowest level. The pooled RR for T2DM for a daily increment of 1 mg of heme iron intake was 1.16 (1.09 to 1.23, P<0.001). Body iron stores, as measured by ferritin, soluble transferrin receptor (sTfR) and the sTfR:ferritin ratio, were significantly associated with the risk of T2DM. The pooled RRs for T2DM in individuals with the highest versus the lowest intake of ferritin levels was 1.70 (1.27-2.27, P<0.001) before adjustment for inflammatory markers and 1.63 (1.03-2.56, P = 0.036) after adjustment. We did not find any significant association of dietary intakes of total iron, non-heme, or supplemental iron intake with T2DM risk.ConclusionHigher heme iron intake and increased body iron stores were significantly associated with a greater risk of T2DM. Dietary total iron, non-heme iron, or supplemental iron intakes were not significantly associated with T2DM risk.

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Section: Discussionmentioning

confidence: 95%

Dietary iron intake, body iron stores, and the risk of type 2 diabetes: a systematic review and meta-analysis

Bao

Rong

et al. 2012

BMC Med

232

180

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“…HH individuals have a 60% chance of developing T2D in their lifetime, compared to 35% in the general population [ 34 ]. Regular phlebotomy temporarily reduces circulating iron burden and blood glucose levels in HH subjects with T2D [ 35 ]. Mouse models of HH reveal that chronic iron overload decreases insulin secretion capacity due to high levels of oxidative stress [ 36 ].…”

Section: Dietary Iron: Too Much Of a Good Thing?mentioning

confidence: 99%

Ironing out the Details: Untangling Dietary Iron and Genetic Background in Diabetes

Miranda

Lawson

2018

Nutrients

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The search for genetic risk factors in type-II diabetes has been hindered by a failure to consider dietary variables. Dietary nutrients impact metabolic disease risk and severity and are essential to maintaining metabolic health. Genetic variation between individuals confers differences in metabolism, which directly impacts response to diet. Most studies attempting to identify genetic risk factors in disease fail to incorporate dietary components, and thus are ill-equipped to capture the breadth of the genome’s impact on metabolism. Understanding how genetic background interacts with nutrients holds the key to predicting and preventing metabolic diseases through the implementation of personalized nutrition. Dysregulation of iron homeostasis is associated with type-II diabetes, but the link between dietary iron and metabolic dysfunction is poorly defined. High iron burden in adipose tissue induces insulin resistance, but the mechanisms underlying adipose iron accumulation remain unknown. Hepcidin controls dietary iron absorption and distribution in metabolic tissues, but it is unknown whether genetic variation influencing hepcidin expression modifies susceptibility to dietary iron-induced insulin resistance. This review highlights discoveries concerning the axis of iron homeostasis and adipose function and suggests that genetic variation underlying dietary iron metabolism is an understudied component of metabolic disease.

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“…Iron reduction by phlebotomy and chelation therapy produced an improvement in glucose tolerance not only in patients with hemochromatosis (Dymock et al, 1972; Inoue et al, 1997), but also in healthy donors. Houschyar et al (2012) reported that reduction of body iron stores through phlebotomy had therapeutic effects in metabolic syndrome patients, including lowered blood pressure and improvement in glycemic control and cardiovascular risks.…”

Section: Iron and Metabolic Syndrome And Diabetesmentioning

confidence: 99%

Epidemiological associations between iron and cardiovascular disease and diabetes

Basuli

Stevens

Torti

et al. 2014

FPHAR

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Disruptions in iron homeostasis are linked to a broad spectrum of chronic conditions including cardiovascular, malignant, metabolic, and neurodegenerative disease. Evidence supporting this contention derives from a variety of analytical approaches, ranging from molecular to population-based studies. This review focuses on key epidemiological studies that assess the relationship between body iron status and chronic diseases, with particular emphasis on atherosclerosis ,metabolic syndrome and diabetes. Multiple surrogates have been used to measure body iron status, including serum ferritin, transferrin saturation, serum iron, and dietary iron intake. The lack of a uniform and standardized means of assessing body iron status has limited the precision of epidemiological associations. Intervention studies using depletion of iron to alter risk have been conducted. Genetic and molecular techniques have helped to explicate the biochemistry of iron metabolism at the molecular level. Plausible explanations for how iron contributes to the pathogenesis of these chronic diseases are beginning to be elucidated. Most evidence supports the hypothesis that excess iron contributes to chronic disease by fostering excess production of free radicals. Overall, epidemiological studies, reinforced by basic science experiments, provide a strong line of evidence supporting the association between iron and elevated risk of cardiovascular disease and diabetes. In this narrative review we attempt to condense the information from existing literature on this topic.

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Recovery of Pancreatic β-cell Function in Hemochromatosis: Combined Treatment With Recombinant Human Erythropoietin and Phlebotomy

Cited by 15 publications

References 5 publications

Dietary iron intake, body iron stores, and the risk of type 2 diabetes: a systematic review and meta-analysis

Dietary iron intake, body iron stores, and the risk of type 2 diabetes: a systematic review and meta-analysis

Ironing out the Details: Untangling Dietary Iron and Genetic Background in Diabetes

Epidemiological associations between iron and cardiovascular disease and diabetes

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