Insulin SecretionNCT05238987
Effect of Taking a Single Tablet of Iron on Insulin Secretion
A study testing Ferrous sulphate in people with Insulin Secretion, run by Christian Medical College, Vellore, India at 1 site in India.
Trial summary
Oral supplementation with highly bioavailable forms of iron, such as ferrous sulphate, is the treatment of choice for iron-deficiency anemia. Iron from ferrous sulphate is efficiently absorbed in the duodenum, resulting in a rapid increase in transferrin saturation and appearance of "free iron" or non-transferrin… Read more about this study
- Who is it for?
- Ages 18 to 60 years, men onlyHealthy volunteers can take part
- Conditions the study is for
- Insulin Secretion
- What is being tested?
- Ferrous sulphate
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 15 participants
- Where
- 1 siteIndia
- Study dates
- 10 Oct 2020to 16 Sep 2021
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 60 years
- Men only
- Healthy volunteers accepted
- Adult
Who may be able to join
- BMI - 18 to 30 kg/m^2
Who cannot join
- Known case of diabetes mellitus/pre-diabetes
- History of chronic inflammatory disease
- Anemia (detection of pallor on examination). Absence of anemia will be confirmed by hemoglobin estimation done at the time of baseline OGTT based on WHO criteria.
- On iron supplementation
- History of any gastrointestinal disorders that might affect absorption of iron/glucose
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Acute Effect of a Single Dose of Oral Iron on Pancreatic Beta Cell Function in Healthy Individuals: a Quasi-experimental Single Arm Before-and-after (Pre-post) Study
Oral supplementation with highly bioavailable forms of iron, such as ferrous sulphate, is the treatment of choice for iron-deficiency anemia. Iron from ferrous sulphate is efficiently absorbed in the duodenum, resulting in a rapid increase in transferrin saturation and appearance of "free iron" or non-transferrin bound iron (NTBI) in blood. NTBI is highly reactive and can catalyze the generation of reactive oxygen species and cause oxidative tissue damage.
Human pancreatic beta cells are known to express ZIP14, a transporter that has been implicated in uptake of NTBI from blood. In vitro and animal studies have shown that iron loading in beta cells can result in impaired insulin secretion. However, there are no human studies that have looked at the acute effects of oral iron intake on insulin secretion.
In this study, we plan to look at the effect of a single oral dose of ferrous sulphate on insulin secretion kinetics in healthy individuals. A single arm before-and-after (pre-post) study design will be used. Consenting individuals who meet the participation criteria will undergo a 75g oral glucose tolerance test (OGTT) to document baseline insulin secretion kinetics. One week later, OGTT will be repeated after administering a single dose of ferrous sulphate (120 mg of elemental iron) 2 hours prior to the test. Iron-induced change in insulin secretion kinetics will be documented. In addition, we will determine changes in glucose tolerance, insulin resistance and insulin clearance rates.
Read the detailed description
Oral iron supplementation is the treatment of choice in patients with iron deficiency anemia. In several developing countries, including India, iron is routinely supplemented to pregnant women, especially during the second and third trimesters of pregnancy owing to the increased iron requirement for the placenta and growing fetus.
Oral administration of iron is preferred to intravenous administration because it is effective, relatively cheap and safe. There are many different oral iron preparations and most of them contain iron in the ferrous form (ferrous sulphate, ferrous fumarate, ferrous gluconate, ferrous ascorbate etc.). Although it has been shown that all these preparations are equally effective in increasing hemoglobin levels, ferrous sulphate, being easily available and economical, is the most prescribed iron preparation.
Iron is absorbed in the duodenum. Dietary iron is usually in the ferric form and must be reduced to the ferrous form prior to absorption. This reduction reaction is catalyzed by duodenal ferrireductases (such as duodenal cytochrome b) and is aided by gastric HCl and other reducing substances in the diet, such as vitamin C (ascorbic acid). Administration of iron in the ferrous form (e.g., ferrous sulphate) circumvents this step, thus making it readily bioavailable. Ferrous iron is transported across the luminal membrane of the enterocytes via divalent metal transporter-1 (DMT-1). Iron is then transported across the basolateral membrane (into blood) by another transporter, ferroportin. Hepcidin, a peptide hormone synthesized and secreted by the liver, binds to and degrades ferroportin, thus reducing intestinal iron absorption.
In the blood, iron is transported bound to the plasma protein, transferrin, which binds iron with high affinity. Transferrin is normally saturated to about 30 to 35% of its total iron binding capacity, leaving a large reserve to bind additional iron. In conditions of iron overload, such as hemochromatosis or in patients with thalassemia, transferrin saturation can increase significantly. When transferrin saturation increases beyond 60% and especially as it approaches 80%, a small but significant amount of iron circulates in blood that is not bound to transferrin. This fraction, called "labile iron" or non-transferrin bound iron (NTBI), is highly reactive and can cause oxidative tissue damage.
NTBI is rapidly cleared from circulation, mainly by hepatocytes. It has been shown that ZIP14 is physiologically the most important transporter that transports NTBI into hepatocytes. Recently, it was shown that ZIP14 is also expressed on human pancreatic beta cells and that it may mediate NTBI uptake by these cells. Several in vitro and animal studies have shown that iron overload impairs pancreatic beta cell function. Patients with hemochromatosis are known to accumulate iron in the beta cells, resulting in diabetes due to decreased insulin secretory capacity. On the other hand, iron chelation or dietary iron restriction improves insulin secretion in mouse models of diabetes. Similarly, iron chelation in hemochromatosis and thalassemia also improved insulin secretion. These studies prove a strong link between increased iron and impaired beta cell function.
It has been shown that, following a single dose of ferrous sulphate (containing 60-100 mg of elemental iron), transferrin saturation increases rapidly and peaks (at ~ 80%) 2 hours after administration. This is associated with a significant increase in NTBI, which also peaks at 2 hours. Given that oral iron administration increases NTBI in blood and that pancreatic beta cells take up NTBI via ZIP14, we hypothesized that oral iron may lead to increased beta cell iron levels which may then cause impaired insulin secretion
In order to test this hypothesis, we plan to conduct a quasi-experimental single arm before-and-after study, where insulin secretion kinetics will be determined at baseline and after a single dose of iron (ferrous sulphate, 120 mg elemental iron) in healthy men.
Healthy male volunteers will be recruited from among the staff of Christian Medical College, Vellore after obtaining written informed consent.Participants will undergo a 75g oral glucose tolerance tests (OGTT) to document baseline insulin secretion kinetics. One week later, the OGTT will be repeated after a single dose of ferrous sulphate (120 mg of elemental iron) given 2 hours before the test. Serum levels of glucose, insulin, C-peptide, serum iron and transferrin saturation will be measured during both OGTT. The effects of iron on insulin secretion kinetics will be documented. In addition, we will determine if changes occur in glucose tolerance, insulin resistance and insulin clearance rates.
- Conditions
- Insulin Secretion
- Being tested
- Ferrous sulphate
- Keywords
- Oral iron, Insulin-Secreting Cells, Diabetes Mellitus
- Medical subject headings
- Diabetes Mellitus
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Ferrous sulphateDietary supplement
Single dose of ferrous sulphate (120 mg of elemental iron)
| Study group | Role | What they receive |
|---|---|---|
| Healthy men (before-and-after (pre-post) study) | Experimental | Partcipants will undergo a 75g oral glucose tolerance test (OGTT) to document baseline insulin secretion kinetics. One week later, OGTT will be repeated after administering a single dose of ferrous sulphate (120 mg of elemental iron) 2 hours prior to the test. Receives: Dietary Supplement: Ferrous sulphate |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change in insulin secretion kinetics
Change in insulin secretion rate as determined by deconvolution of C-peptide levels in blood during an oral glucose tolerance test based on a previously published mathematical model (Van Cauter et al., 1992).
Measured: 2 hours from intake of 120 mg of elemental iron
Change in disposition index
Disposition index is a measure of beta-cell function which is calculated as a product of insulin sensitivity and insulin secretion during an oral glucose tolerance test
Measured: 2 hours from intake of 120 mg of elemental iron
Change in insulinogenic index
A measure of beta-cell function which calculates the increase in insulin secretion in response to increase in glucose concentration during an oral glucose tolerance test
Measured: 2 hours from intake of 120 mg of elemental iron
Secondary outcomes (3)
Change in glucose tolerance
Glucose tolerance will be determined by calculating the area under the curve (AUC) of glucose levels during oral glucose tolerance test
Measured: 2 hours from intake of 120 mg of elemental iron
Change in insulin sensitivity
Insulin sensitivity which is a measure of insulin action will be calculated using the Matsuda index (Matsuda and DeFronzo, 1999)
Measured: 2 hours from intake of 120 mg of elemental iron
Change in insulin clearance rate
Insulin clearance rate which is a measure of rate of disappearance of insulin from the blood will be calculated as described previously (Castillo et al., 1994)
Measured: 2 hours from intake of 120 mg of elemental iron
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted14 Feb 2022
- Study start10 Oct 2020
- Primary completion16 Sep 2021
- Study completion16 Sep 2021
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (22)Papers the sponsor has linked to this study.
- Other trials for Insulin SecretionStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Not applicable
- Intervention model
- Single group
- Model description
- Quasi-experimental single arm before-and-after (pre-post) study.
- Masking
- None (open label)
- Enrolment
- 15 participants (actual)
Sponsor and investigators
- Lead sponsor
- Christian Medical College, Vellore, India
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Padmanaban Venkatesan, Christian Medical College, Vellore, India
- Investigators
- Padmanaban Venkatesan, M.D., Principal investigator, Christian Medical College, Vellore, IndiaJoe Varghese, M.D.,PhD, Principal investigator, Christian Medical College, Vellore, India
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05238987
- Sponsor's protocol ID
- IRB min.13294 Dt.26.08.2020
- Status last verified
- Feb 2022
- First submitted
- 5 Feb 2022
- Last updated
- 2 Mar 2022
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Abraham D, Rogers J, Gault P, Kushner JP, McClain DA. Increased insulin secretory capacity but decreased insulin sensitivity after correction of iron overload by phlebotomy in hereditary haemochromatosis. Diabetologia. 2006 Nov;49(11):2546-51. doi: 10.1007/s00125-006-0445-7. Epub 2006 Sep 22.
PubMed 17019598Auerbach M, Adamson JW. How we diagnose and treat iron deficiency anemia. Am J Hematol. 2016 Jan;91(1):31-8. doi: 10.1002/ajh.24201. Epub 2015 Nov 17.
PubMed 26408108Backe MB, Moen IW, Ellervik C, Hansen JB, Mandrup-Poulsen T. Iron Regulation of Pancreatic Beta-Cell Functions and Oxidative Stress. Annu Rev Nutr. 2016 Jul 17;36:241-73. doi: 10.1146/annurev-nutr-071715-050939. Epub 2016 May 4.
PubMed 27146016Brissot P, Ropert M, Le Lan C, Loreal O. Non-transferrin bound iron: a key role in iron overload and iron toxicity. Biochim Biophys Acta. 2012 Mar;1820(3):403-10. doi: 10.1016/j.bbagen.2011.07.014. Epub 2011 Aug 9.
PubMed 21855608Castillo MJ, Scheen AJ, Letiexhe MR, Lefebvre PJ. How to measure insulin clearance. Diabetes Metab Rev. 1994 Jul;10(2):119-50. doi: 10.1002/dmr.5610100205. No abstract available.
PubMed 7956676Coffey R, Knutson MD. The plasma membrane metal-ion transporter ZIP14 contributes to nontransferrin-bound iron uptake by human beta-cells. Am J Physiol Cell Physiol. 2017 Feb 1;312(2):C169-C175. doi: 10.1152/ajpcell.00116.2016. Epub 2016 Nov 30.
PubMed 27903581Cooksey RC, Jones D, Gabrielsen S, Huang J, Simcox JA, Luo B, Soesanto Y, Rienhoff H, Abel ED, McClain DA. Dietary iron restriction or iron chelation protects from diabetes and loss of beta-cell function in the obese (ob/ob lep-/-) mouse. Am J Physiol Endocrinol Metab. 2010 Jun;298(6):E1236-43. doi: 10.1152/ajpendo.00022.2010. Epub 2010 Mar 30.
PubMed 20354157Dresow B, Petersen D, Fischer R, Nielsen P. Non-transferrin-bound iron in plasma following administration of oral iron drugs. Biometals. 2008 Jun;21(3):273-6. doi: 10.1007/s10534-007-9116-5. Epub 2007 Sep 13.
PubMed 17851733Farmaki K, Angelopoulos N, Anagnostopoulos G, Gotsis E, Rombopoulos G, Tolis G. Effect of enhanced iron chelation therapy on glucose metabolism in patients with beta-thalassaemia major. Br J Haematol. 2006 Aug;134(4):438-44. doi: 10.1111/j.1365-2141.2006.06203.x. Epub 2006 Jul 4.
PubMed 16822284Fuqua BK, Vulpe CD, Anderson GJ. Intestinal iron absorption. J Trace Elem Med Biol. 2012 Jun;26(2-3):115-9. doi: 10.1016/j.jtemb.2012.03.015. Epub 2012 May 8.
PubMed 22575541Geisser P, Burckhardt S. The pharmacokinetics and pharmacodynamics of iron preparations. Pharmaceutics. 2011 Jan 4;3(1):12-33. doi: 10.3390/pharmaceutics3010012.
PubMed 24310424Goddard AF, James MW, McIntyre AS, Scott BB; British Society of Gastroenterology. Guidelines for the management of iron deficiency anaemia. Gut. 2011 Oct;60(10):1309-16. doi: 10.1136/gut.2010.228874. Epub 2011 May 11.
PubMed 21561874Hansen JB, Tonnesen MF, Madsen AN, Hagedorn PH, Friberg J, Grunnet LG, Heller RS, Nielsen AO, Storling J, Baeyens L, Anker-Kitai L, Qvortrup K, Bouwens L, Efrat S, Aalund M, Andrews NC, Billestrup N, Karlsen AE, Holst B, Pociot F, Mandrup-Poulsen T. Divalent metal transporter 1 regulates iron-mediated ROS and pancreatic beta cell fate in response to cytokines. Cell Metab. 2012 Oct 3;16(4):449-61. doi: 10.1016/j.cmet.2012.09.001. Epub 2012 Sep 20.
PubMed 23000401Jenkitkasemwong S, Wang CY, Coffey R, Zhang W, Chan A, Biel T, Kim JS, Hojyo S, Fukada T, Knutson MD. SLC39A14 Is Required for the Development of Hepatocellular Iron Overload in Murine Models of Hereditary Hemochromatosis. Cell Metab. 2015 Jul 7;22(1):138-50. doi: 10.1016/j.cmet.2015.05.002. Epub 2015 May 28.
PubMed 26028554Kapil U, Kapil R, Gupta A. National Iron Plus Initiative: Current status & future strategy. Indian J Med Res. 2019 Sep;150(3):239-247. doi: 10.4103/ijmr.IJMR_1782_18.
PubMed 31719294
Study at a glance
From the registry record, last updated by the sponsor on 2 Mar 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Acute Effect of a Single Dose of Oral Iron on Pancreatic Beta Cell Function in Healthy Individuals: a Quasi-experimental Single Arm Before-and-after (Pre-post) Study
- ClinicalTrials.gov ID
- NCT05238987
- Acronym / sponsor ID
- IRB min.13294 Dt.26.08.2020
- Conditions
- Insulin Secretion
- Keywords
- Oral iron, Insulin-Secreting Cells, Diabetes Mellitus
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 15 participants (actual)
- Lead sponsor
- Christian Medical College, Vellore, IndiaUniversity, hospital or other
- Study start
- 10 Oct 2020 (actual)
- Primary completion
- 16 Sep 2021 (actual)
- Study completion
- 16 Sep 2021 (actual)
- First posted
- 14 Feb 2022 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Oral supplementation with highly bioavailable forms of iron, such as ferrous sulphate, is the treatment of choice for iron-deficiency anemia. Iron from ferrous sulphate is efficiently absorbed in the duodenum, resulting in a rapid increase in transferrin saturation and appearance of "free iron" or non-transferrin bound iron (NTBI) in blood. NTBI is highly reactive and can catalyze the generation of reactive oxygen species and cause oxidative tissue damage.
Human pancreatic beta cells are known to express ZIP14, a transporter that has been implicated in uptake of NTBI from blood. In vitro and animal studies have shown that iron loading in beta cells can result in impaired insulin secretion. However, there are no human studies that have looked at the acute effects of oral iron intake on insulin secretion.
In this study, we plan to look at the effect of a single oral dose of ferrous sulphate on insulin secretion kinetics in healthy individuals. A single arm before-and-after (pre-post) study design will be used. Consenting individuals who meet the participation criteria will undergo a 75g oral glucose tolerance test (OGTT) to document baseline insulin secretion kinetics. One week later, OGTT will be repeated after administering a single dose of ferrous sulphate (120 mg of elemental iron) 2 hours prior to the test. Iron-induced change in insulin secretion kinetics will be documented. In addition, we will determine changes in glucose tolerance, insulin resistance and insulin clearance rates.
Detailed description
Oral iron supplementation is the treatment of choice in patients with iron deficiency anemia. In several developing countries, including India, iron is routinely supplemented to pregnant women, especially during the second and third trimesters of pregnancy owing to the increased iron requirement for the placenta and growing fetus.
Oral administration of iron is preferred to intravenous administration because it is effective, relatively cheap and safe. There are many different oral iron preparations and most of them contain iron in the ferrous form (ferrous sulphate, ferrous fumarate, ferrous gluconate, ferrous ascorbate etc.). Although it has been shown that all these preparations are equally effective in increasing hemoglobin levels, ferrous sulphate, being easily available and economical, is the most prescribed iron preparation.
Iron is absorbed in the duodenum. Dietary iron is usually in the ferric form and must be reduced to the ferrous form prior to absorption. This reduction reaction is catalyzed by duodenal ferrireductases (such as duodenal cytochrome b) and is aided by gastric HCl and other reducing substances in the diet, such as vitamin C (ascorbic acid). Administration of iron in the ferrous form (e.g., ferrous sulphate) circumvents this step, thus making it readily bioavailable. Ferrous iron is transported across the luminal membrane of the enterocytes via divalent metal transporter-1 (DMT-1). Iron is then transported across the basolateral membrane (into blood) by another transporter, ferroportin. Hepcidin, a peptide hormone synthesized and secreted by the liver, binds to and degrades ferroportin, thus reducing intestinal iron absorption.
In the blood, iron is transported bound to the plasma protein, transferrin, which binds iron with high affinity. Transferrin is normally saturated to about 30 to 35% of its total iron binding capacity, leaving a large reserve to bind additional iron. In conditions of iron overload, such as hemochromatosis or in patients with thalassemia, transferrin saturation can increase significantly. When transferrin saturation increases beyond 60% and especially as it approaches 80%, a small but significant amount of iron circulates in blood that is not bound to transferrin. This fraction, called "labile iron" or non-transferrin bound iron (NTBI), is highly reactive and can cause oxidative tissue damage.
NTBI is rapidly cleared from circulation, mainly by hepatocytes. It has been shown that ZIP14 is physiologically the most important transporter that transports NTBI into hepatocytes. Recently, it was shown that ZIP14 is also expressed on human pancreatic beta cells and that it may mediate NTBI uptake by these cells. Several in vitro and animal studies have shown that iron overload impairs pancreatic beta cell function. Patients with hemochromatosis are known to accumulate iron in the beta cells, resulting in diabetes due to decreased insulin secretory capacity. On the other hand, iron chelation or dietary iron restriction improves insulin secretion in mouse models of diabetes. Similarly, iron chelation in hemochromatosis and thalassemia also improved insulin secretion. These studies prove a strong link between increased iron and impaired beta cell function.
It has been shown that, following a single dose of ferrous sulphate (containing 60-100 mg of elemental iron), transferrin saturation increases rapidly and peaks (at ~ 80%) 2 hours after administration. This is associated with a significant increase in NTBI, which also peaks at 2 hours. Given that oral iron administration increases NTBI in blood and that pancreatic beta cells take up NTBI via ZIP14, we hypothesized that oral iron may lead to increased beta cell iron levels which may then cause impaired insulin secretion
In order to test this hypothesis, we plan to conduct a quasi-experimental single arm before-and-after study, where insulin secretion kinetics will be determined at baseline and after a single dose of iron (ferrous sulphate, 120 mg elemental iron) in healthy men.
Healthy male volunteers will be recruited from among the staff of Christian Medical College, Vellore after obtaining written informed consent.Participants will undergo a 75g oral glucose tolerance tests (OGTT) to document baseline insulin secretion kinetics. One week later, the OGTT will be repeated after a single dose of ferrous sulphate (120 mg of elemental iron) given 2 hours before the test. Serum levels of glucose, insulin, C-peptide, serum iron and transferrin saturation will be measured during both OGTT. The effects of iron on insulin secretion kinetics will be documented. In addition, we will determine if changes occur in glucose tolerance, insulin resistance and insulin clearance rates.
Study design
- Primary purpose
- Basic science
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
- Model description
- Quasi-experimental single arm before-and-after (pre-post) study.
| Arm | Type | Receives |
|---|---|---|
| Healthy men (before-and-after (pre-post) study) | Experimental | Dietary Supplement: Ferrous sulphatePartcipants will undergo a 75g oral glucose tolerance test (OGTT) to document baseline insulin secretion kinetics. One week later, OGTT will be repeated after administering a single dose of ferrous sulphate (120 mg of elemental iron) 2 hours prior to the test. |
Who may qualify
- Ages
- 18 to 60 years
- Sex
- Male only
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (1 listed)
- BMI - 18 to 30 kg/m^2
Key exclusion criteria (5 listed)
- Known case of diabetes mellitus/pre-diabetes
- History of chronic inflammatory disease
- Anemia (detection of pallor on examination). Absence of anemia will be confirmed by hemoglobin estimation done at the time of baseline OGTT based on WHO criteria.
- On iron supplementation
- History of any gastrointestinal disorders that might affect absorption of iron/glucose
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Ferrous sulphateSingle dose of ferrous sulphate (120 mg of elemental iron) | Dietary supplement | Healthy men (before-and-after (pre-post) study) |
Primary outcome
Change in insulin secretion kinetics
Time frame: 2 hours from intake of 120 mg of elemental iron
Change in insulin secretion rate as determined by deconvolution of C-peptide levels in blood during an oral glucose tolerance test based on a previously published mathematical model (Van Cauter et al., 1992).
Change in disposition index
Time frame: 2 hours from intake of 120 mg of elemental iron
Disposition index is a measure of beta-cell function which is calculated as a product of insulin sensitivity and insulin secretion during an oral glucose tolerance test
Change in insulinogenic index
Time frame: 2 hours from intake of 120 mg of elemental iron
A measure of beta-cell function which calculates the increase in insulin secretion in response to increase in glucose concentration during an oral glucose tolerance test
3 secondary outcomes
Change in glucose tolerance
Time frame: 2 hours from intake of 120 mg of elemental iron
Change in insulin sensitivity
Time frame: 2 hours from intake of 120 mg of elemental iron
Change in insulin clearance rate
Time frame: 2 hours from intake of 120 mg of elemental iron
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 2 Mar 2022.
- Background: PubMed 17019598Abraham D, Rogers J, Gault P, Kushner JP, McClain DA. Increased insulin secretory capacity but decreased insulin sensitivity after correction of iron overload by phlebotomy in hereditary haemochromatosis. Diabetologia. 2006 Nov;49(11):2546-51. doi: 10.1007/s00125-006-0445-7. Epub 2006 Sep 22.
- Background: PubMed 26408108Auerbach M, Adamson JW. How we diagnose and treat iron deficiency anemia. Am J Hematol. 2016 Jan;91(1):31-8. doi: 10.1002/ajh.24201. Epub 2015 Nov 17.
- Background: PubMed 27146016Backe MB, Moen IW, Ellervik C, Hansen JB, Mandrup-Poulsen T. Iron Regulation of Pancreatic Beta-Cell Functions and Oxidative Stress. Annu Rev Nutr. 2016 Jul 17;36:241-73. doi: 10.1146/annurev-nutr-071715-050939. Epub 2016 May 4.
- Background: PubMed 21855608Brissot P, Ropert M, Le Lan C, Loreal O. Non-transferrin bound iron: a key role in iron overload and iron toxicity. Biochim Biophys Acta. 2012 Mar;1820(3):403-10. doi: 10.1016/j.bbagen.2011.07.014. Epub 2011 Aug 9.
- Background: PubMed 7956676Castillo MJ, Scheen AJ, Letiexhe MR, Lefebvre PJ. How to measure insulin clearance. Diabetes Metab Rev. 1994 Jul;10(2):119-50. doi: 10.1002/dmr.5610100205. No abstract available.
- Background: PubMed 27903581Coffey R, Knutson MD. The plasma membrane metal-ion transporter ZIP14 contributes to nontransferrin-bound iron uptake by human beta-cells. Am J Physiol Cell Physiol. 2017 Feb 1;312(2):C169-C175. doi: 10.1152/ajpcell.00116.2016. Epub 2016 Nov 30.
- Background: PubMed 20354157Cooksey RC, Jones D, Gabrielsen S, Huang J, Simcox JA, Luo B, Soesanto Y, Rienhoff H, Abel ED, McClain DA. Dietary iron restriction or iron chelation protects from diabetes and loss of beta-cell function in the obese (ob/ob lep-/-) mouse. Am J Physiol Endocrinol Metab. 2010 Jun;298(6):E1236-43. doi: 10.1152/ajpendo.00022.2010. Epub 2010 Mar 30.
- Background: PubMed 17851733Dresow B, Petersen D, Fischer R, Nielsen P. Non-transferrin-bound iron in plasma following administration of oral iron drugs. Biometals. 2008 Jun;21(3):273-6. doi: 10.1007/s10534-007-9116-5. Epub 2007 Sep 13.
- Background: PubMed 16822284Farmaki K, Angelopoulos N, Anagnostopoulos G, Gotsis E, Rombopoulos G, Tolis G. Effect of enhanced iron chelation therapy on glucose metabolism in patients with beta-thalassaemia major. Br J Haematol. 2006 Aug;134(4):438-44. doi: 10.1111/j.1365-2141.2006.06203.x. Epub 2006 Jul 4.
- Background: PubMed 22575541Fuqua BK, Vulpe CD, Anderson GJ. Intestinal iron absorption. J Trace Elem Med Biol. 2012 Jun;26(2-3):115-9. doi: 10.1016/j.jtemb.2012.03.015. Epub 2012 May 8.
- Background: PubMed 24310424Geisser P, Burckhardt S. The pharmacokinetics and pharmacodynamics of iron preparations. Pharmaceutics. 2011 Jan 4;3(1):12-33. doi: 10.3390/pharmaceutics3010012.
- Background: PubMed 21561874Goddard AF, James MW, McIntyre AS, Scott BB; British Society of Gastroenterology. Guidelines for the management of iron deficiency anaemia. Gut. 2011 Oct;60(10):1309-16. doi: 10.1136/gut.2010.228874. Epub 2011 May 11.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Padmanaban Venkatesan, M.D. principal investigator
Christian Medical College, Vellore, India
Joe Varghese, M.D.,PhD principal investigator
Christian Medical College, Vellore, India
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Ferrous sulphate in people with Insulin Secretion, run by Christian Medical College, Vellore, India at 1 site in India.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 5 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 2 Mar 2022. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in India. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Change in insulin secretion kinetics (time frame: 2 hours from intake of 120 mg of elemental iron). The study lists 3 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05238987, which also lists 22 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 2 Mar 2022.