Insulin ResistanceOVEREATNCT03369145
High-fat Overfeeding, Hepatokines and Appetite Regulation
A study testing High-fat diet in people with Insulin Resistance and Type2 Diabetes Mellitus, run by Loughborough University at 2 sites in United Kingdom.
Trial summary
The present study will investigate the effect of high-fat overfeeding on a group of liver-secreted proteins linked to worsened blood sugar control, as well as proteins involved in appetite control. Read more about this study
- Who is it for?
- Ages 18 to 40 years, men onlyHealthy volunteers can take part
- Conditions the study is for
- Insulin Resistance, Type2 Diabetes Mellitus, Non-Alcoholic Fatty Liver Disease
- What is being tested?
- High-fat diet
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 12 participants
- Where
- 2 sitesUnited Kingdom
- Study dates
- 11 Dec 2017to 31 Jul 2018
- 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 40 years
- Men only
- Healthy volunteers accepted
- Adult
Who may be able to join
- Recreationally active - ≤ 2 structured exercise sessions per week
- BMI between 18.5 - 27.9 kg/m2
- Body fat percentage < 20%
- Metabolically healthy - No known cardiovascular or metabolic disease such as diabetes, respiratory or heart disease.
- Non-smoker
- Weight stable in the past 6 months
- Normal fasting blood glucose levels (3.6 - 5.5 mmol/l)
Who cannot join
- Contraindications to exercise
- Needle Phobia
Trial locations and contacts
2 sites in 1 country.
United Kingdom2 sites
National Centre for Sport and Exercise Medicine, Loughborough University
Loughborough, Leicestershire, LE11 3TU
Clifton Campus, Nottingham Trent University
Nottingham, Nottinghamshire, NG1 4FQ
About this study
Official title: Influence of High-fat Overfeeding on Circulating Hepatokine Concentrations: a Randomised Crossover Study
The present study will investigate the effect of high-fat overfeeding on a group of liver-secreted proteins linked to worsened blood sugar control, as well as proteins involved in appetite control. Participants will consume both a high-fat diet, consisting of 50% extra calories above their daily required intake, and a control diet, consisting of their normal 'habitual' diet, with each diet lasting seven days. The diets will be undertaken in a randomised order, with a period of three weeks separating the two diets. Blood samples will be taken before and after each diet to measure blood sugar control. Further blood samples will also be taken 24 hours and 72 hours into each diet to see how levels of the liver and appetite-regulating proteins change over the course of the seven days.
It is expected that blood sugar control will be worsened by the high-fat diet and this will be accompanied by increases in levels of the liver-secreted proteins and an impaired release of the appetite-regulating proteins into the blood.
Read the detailed description
In recent years, researchers have identified a number of liver-secreted proteins, termed "hepatokines", which are thought to play an important role in inter-organ crosstalk between the liver and other metabolically active tissues such as skeletal muscle and adipose tissue. Specifically, previous studies have demonstrated that hepatokines contribute to whole body glucose and lipid homeostasis through acting in an endocrine-like fashion. Understanding how circulating concentrations of these hepatokines can be manipulated in humans is essential, as impaired blood glucose and lipid control is a key feature of metabolic diseases, such as type 2 diabetes and non-alcoholic fatty liver disease.
Previous research at Loughborough University has found that acute high-fat overfeeding for up to seven days can impair glycaemic control; however, the exact mechanisms responsible for these detrimental changes are not fully understood. Based upon previous evidence that hepatokine production is nutritionally modulated, the investigators believe that changes in hepatokine production may play a role in the detrimental metabolic effects seen following short-term, high-fat overfeeding which has implications for long-term metabolic health.
Appetite regulation is also thought to play a role in the pathophysiology of obesity and insulin resistance, as the impaired secretion of several appetite regulatory hormones in both fasting and postprandial conditions has been observed in obesity, which is characterised by an chronic excessive energy intake. Therefore, the investigators are also interested to examine the appetite regulatory hormone response to short-term, high-fat overfeeding.
The present study is a randomised, controlled, crossover study in which twelve recreationally active, healthy males will consume both a hypercaloric, high-fat diet (consisting of 50% extra energy above the daily requirement, 65% of which is fat) and a control diet (the participants' habitual diet) in a randomised fashion. A three-week washout period will separate the two diets in order to remove any lasting effects confounding the subsequent diet.
Following a prescreening session in which anthropometric data will be collected, participants will commence their first dietary condition. An oral glucose tolerance test will be performed before and after the two diets to measure changes in glycaemic control/whole body insulin sensitivity. Further blood samples will be taken 24 hours and 72 hours after commencing the diets in order to observe the time course of any changes in circulating hepatokine and appetite hormone concentrations. Physical activity will also be monitored for the duration of the two dietary conditions to ensure that habitual physical activity levels are maintained.
- Being tested
- High-fat diet
- Keywords
- Hepatokines, High Fat Diet, Glycaemic Control, Fibroblast Growth Factor 21, Leukocyte Cell-derived Chemotaxin 2, Fetuin-A, Appetite, Ghrelin, Peptide YY
- Medical subject headings
- Insulin Resistance, Non-alcoholic Fatty Liver Disease, Obesity
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
High-fat dietDietary supplement
The high-fat diet will provide 7 days of overfeeding comprising of: +50% extra calories above the daily required intake, 65% of which is fat.
| Study group | Role | What they receive |
|---|---|---|
| High-fat diet | Experimental | Participants will consume a hypercaloric, high-fat diet. Participants will be provided with all the food during the week and will be instructed to consume all of the foods provided and no extra calorie containing food or drink. In the event of leftover food, participants will be asked to return the food for measurement and subsequent subtraction from their total energy intake. Receives: Dietary Supplement: High-fat diet |
| Control diet | No intervention | Participants will consume their normal 'habitual' diet for seven days which will be compared to their habitual diet recorded by a three day food diary before commencing the two diets. Participants will be instructed to carry on as normal and eat their usual diet and this period will be used as a comparator to the high-fat diet. They will also be told to record their food intake for 3 days during the diet to quantify their control diet. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Leukocyte cell-derived chemotaxin 2 (LECT2)
Time-course of LECT2 plasma concentrations across the 7-day dietary interventions
Measured: Baseline, 1 day, 3 days, 7 days
Secondary outcomes (17)
Fibroblast growth factor 21 (FGF21)
Time-course of FGF21 plasma concentrations across the 7-day dietary interventions
Measured: Baseline, 1 day, 3 days, 7 days
Fetuin-A
Time-course of Fetuin-A plasma concentrations across the 7-day dietary interventions
Measured: Baseline, 1 day, 3 days, 7 days
Acylated ghrelin
Time-course of acylated ghrelin plasma concentrations across the 7-day dietary interventions
Measured: Baseline, 1 day, 3 days, 7 days
Peptide YY (PYY)
Time-course of PYY plasma concentrations across the 7-day dietary interventions
Measured: Baseline, 1 day, 3 days, 7 days
C-Terminal Telopeptide of Type 1 Collagen (CTX)
Time-course of CTX plasma concentrations across the 7-day dietary interventions
Measured: Baseline, 1 day, 3 days, 7 days
N-Terminal Propeptide of Type 1 Procollagen (P1NP)
Time-course of P1NP plasma concentrations across the 7-day dietary interventions
Measured: Baseline, 1 day, 3 days, 7 days
Visual Analogue Scale for Subjective Ratings of Appetite
Time-course of subjective ratings of hunger across the 7-day dietary interventions, measured using an appetite visual analogue scale. The scale is divided into subscales of different appetite perceptions including: hunger, fullness, satisfaction and prospective food consumption. Each subscale is rated on a 100mm scale (i.e. from 0 - 100), with a rating of 100 fully supporting the perception and a rating of 0 fully opposing the perception.
Measured: Baseline, 1 day, 3 days, 7 days
Subjective food preference
Time-course of subjective food preference across the 7-day dietary interventions, measured using the Leeds Food Preference Questionnaire.
Measured: Baseline, 1 day, 3 days, 7 days
Whole-body insulin sensitivity
Changes in whole-body insulin sensitivity using the Matsuda Index, calculated from plasma glucose and insulin concentrations during the oral glucose tolerance test
Measured: Baseline, 7 Days
Homeostasis model assessment of insulin resistance (HOMA-IR)
Changes in HOMA-IR (a marker of hepatic insulin resistance) using baseline concentrations of plasma glucose and insulin.
Measured: Baseline, 1 day, 3 days, 7 days
Adipose tissue insulin resistance (ADIPO-IR)
Changes in ADIPO-IR using baseline concentrations of plasma insulin and non-esterified free fatty acids.
Measured: Baseline, 1 day, 3 days, 7 days
Physical activity and sedentary behaviour
Amounts of sitting time, standing time, light activity and moderate-vigorous activity will be measured across the duration of each diets to compare between the two. This will be Measured using Acitgraph and ActivPAL monitors.
Measured: 7 days (per diet)
Resting Metabolic Rate
Changes in resting metabolic rate in response to the diets will be measured using indirect calorimetry and estimated using the Haldane transformation.
Measured: Baseline, 7 Days
Fat Oxidation
Changes in fat oxidation in response to the diets will be measured using indirect calorimetry and estimated using the Haldane transformation.
Measured: Baseline, 7 Days
Blood pressure
Changes in blood pressure (systolic and diastolic) across the two dietary interventions will be measured using an automated pressure cuff.
Measured: Baseline, 1 day, 3 days, 7 days
Body weight
Changes in body weight across the two dietary interventions.
Measured: Baseline, 1 day, 3 days, 7 days
Body fat percentage
Changes in body fat percentage across the two dietary interventions using bioelectrical impedance analysis.
Measured: Baseline, 7 Days
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted11 Dec 2017
- Study start11 Dec 2017
- Primary completion31 Jul 2018
- Study completion31 Jul 2018
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (10)Papers the sponsor has linked to this study.
- Other trials for Insulin ResistanceStudies 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
- Randomised
- Intervention model
- Crossover
- Model description
- The study design is a randomised, controlled, crossover design in which participants undertake two 7-day dietary conditions in a randomised order with a three week washout period in between.
- Masking
- None (open label)
- Enrolment
- 12 participants (actual)
Sponsor and investigators
- Lead sponsor
- Loughborough University
- Sponsor type
- University, hospital or other
- Collaborators
- Nottingham Trent University, Nottingham University Hospitals NHS Trust
- Responsible party
- Principal investigator, Scott Willis, Loughborough University
- Investigators
- James A King, PhD, Principal investigator, Loughborough UniversityScott A Willis, MSc, Principal investigator, Loughborough University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03369145
- Sponsor's protocol ID
- R17-P144
- Acronym
- OVEREAT
- Status last verified
- Feb 2019
- First submitted
- 20 Nov 2017
- Last updated
- 18 Feb 2019
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Badman MK, Pissios P, Kennedy AR, Koukos G, Flier JS, Maratos-Flier E. Hepatic fibroblast growth factor 21 is regulated by PPARalpha and is a key mediator of hepatic lipid metabolism in ketotic states. Cell Metab. 2007 Jun;5(6):426-37. doi: 10.1016/j.cmet.2007.05.002.
PubMed 17550778Dasgupta S, Bhattacharya S, Biswas A, Majumdar SS, Mukhopadhyay S, Ray S, Bhattacharya S. NF-kappaB mediates lipid-induced fetuin-A expression in hepatocytes that impairs adipocyte function effecting insulin resistance. Biochem J. 2010 Aug 1;429(3):451-62. doi: 10.1042/BJ20100330.
PubMed 20482516Groop LC. Insulin resistance: the fundamental trigger of type 2 diabetes. Diabetes Obes Metab. 1999 May;1 Suppl 1:S1-7. doi: 10.1046/j.1463-1326.1999.0010s1001.x.
PubMed 11220283Hulston CJ, Churnside AA, Venables MC. Probiotic supplementation prevents high-fat, overfeeding-induced insulin resistance in human subjects. Br J Nutr. 2015 Feb 28;113(4):596-602. doi: 10.1017/S0007114514004097. Epub 2015 Jan 29.
PubMed 25630516Lan F, Misu H, Chikamoto K, Takayama H, Kikuchi A, Mohri K, Takata N, Hayashi H, Matsuzawa-Nagata N, Takeshita Y, Noda H, Matsumoto Y, Ota T, Nagano T, Nakagen M, Miyamoto K, Takatsuki K, Seo T, Iwayama K, Tokuyama K, Matsugo S, Tang H, Saito Y, Yamagoe S, Kaneko S, Takamura T. LECT2 functions as a hepatokine that links obesity to skeletal muscle insulin resistance. Diabetes. 2014 May;63(5):1649-64. doi: 10.2337/db13-0728. Epub 2014 Jan 29.
PubMed 24478397Meex RCR, Watt MJ. Hepatokines: linking nonalcoholic fatty liver disease and insulin resistance. Nat Rev Endocrinol. 2017 Sep;13(9):509-520. doi: 10.1038/nrendo.2017.56. Epub 2017 Jun 9.
PubMed 28621339Parry SA, Smith JR, Corbett TR, Woods RM, Hulston CJ. Short-term, high-fat overfeeding impairs glycaemic control but does not alter gut hormone responses to a mixed meal tolerance test in healthy, normal-weight individuals. Br J Nutr. 2017 Jan;117(1):48-55. doi: 10.1017/S0007114516004475. Epub 2017 Jan 24.
PubMed 28115026Uebanso T, Taketani Y, Yamamoto H, Amo K, Ominami H, Arai H, Takei Y, Masuda M, Tanimura A, Harada N, Yamanaka-Okumura H, Takeda E. Paradoxical regulation of human FGF21 by both fasting and feeding signals: is FGF21 a nutritional adaptation factor? PLoS One. 2011;6(8):e22976. doi: 10.1371/journal.pone.0022976. Epub 2011 Aug 1.
PubMed 21829679Lean ME, Malkova D. Altered gut and adipose tissue hormones in overweight and obese individuals: cause or consequence? Int J Obes (Lond). 2016 Apr;40(4):622-32. doi: 10.1038/ijo.2015.220. Epub 2015 Oct 26.
PubMed 26499438Willis SA, Sargeant JA, Yates T, Takamura T, Takayama H, Gupta V, Brittain E, Crawford J, Parry SA, Thackray AE, Varela-Mato V, Stensel DJ, Woods RM, Hulston CJ, Aithal GP, King JA. Acute Hyperenergetic, High-Fat Feeding Increases Circulating FGF21, LECT2, and Fetuin-A in Healthy Men. J Nutr. 2020 May 1;150(5):1076-1085. doi: 10.1093/jn/nxz333.
PubMed 31919514
Study at a glance
From the registry record, last updated by the sponsor on 18 Feb 2019. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Influence of High-fat Overfeeding on Circulating Hepatokine Concentrations: a Randomised Crossover Study
- ClinicalTrials.gov ID
- NCT03369145
- Acronym / sponsor ID
- OVEREAT / R17-P144
- Keywords
- Hepatokines, High Fat Diet, Glycaemic Control, Fibroblast Growth Factor 21, Leukocyte Cell-derived Chemotaxin 2, Fetuin-A, Appetite, Ghrelin
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 12 participants (actual)
- Lead sponsor
- Loughborough UniversityUniversity, hospital or other
- Collaborators
- Nottingham Trent University, Nottingham University Hospitals NHS Trust
- Study start
- 11 Dec 2017 (actual)
- Primary completion
- 31 Jul 2018 (actual)
- Study completion
- 31 Jul 2018 (actual)
- First posted
- 11 Dec 2017 (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.
The present study will investigate the effect of high-fat overfeeding on a group of liver-secreted proteins linked to worsened blood sugar control, as well as proteins involved in appetite control. Participants will consume both a high-fat diet, consisting of 50% extra calories above their daily required intake, and a control diet, consisting of their normal 'habitual' diet, with each diet lasting seven days. The diets will be undertaken in a randomised order, with a period of three weeks separating the two diets. Blood samples will be taken before and after each diet to measure blood sugar control. Further blood samples will also be taken 24 hours and 72 hours into each diet to see how levels of the liver and appetite-regulating proteins change over the course of the seven days.
It is expected that blood sugar control will be worsened by the high-fat diet and this will be accompanied by increases in levels of the liver-secreted proteins and an impaired release of the appetite-regulating proteins into the blood.
Detailed description
In recent years, researchers have identified a number of liver-secreted proteins, termed "hepatokines", which are thought to play an important role in inter-organ crosstalk between the liver and other metabolically active tissues such as skeletal muscle and adipose tissue. Specifically, previous studies have demonstrated that hepatokines contribute to whole body glucose and lipid homeostasis through acting in an endocrine-like fashion. Understanding how circulating concentrations of these hepatokines can be manipulated in humans is essential, as impaired blood glucose and lipid control is a key feature of metabolic diseases, such as type 2 diabetes and non-alcoholic fatty liver disease.
Previous research at Loughborough University has found that acute high-fat overfeeding for up to seven days can impair glycaemic control; however, the exact mechanisms responsible for these detrimental changes are not fully understood. Based upon previous evidence that hepatokine production is nutritionally modulated, the investigators believe that changes in hepatokine production may play a role in the detrimental metabolic effects seen following short-term, high-fat overfeeding which has implications for long-term metabolic health.
Appetite regulation is also thought to play a role in the pathophysiology of obesity and insulin resistance, as the impaired secretion of several appetite regulatory hormones in both fasting and postprandial conditions has been observed in obesity, which is characterised by an chronic excessive energy intake. Therefore, the investigators are also interested to examine the appetite regulatory hormone response to short-term, high-fat overfeeding.
The present study is a randomised, controlled, crossover study in which twelve recreationally active, healthy males will consume both a hypercaloric, high-fat diet (consisting of 50% extra energy above the daily requirement, 65% of which is fat) and a control diet (the participants' habitual diet) in a randomised fashion. A three-week washout period will separate the two diets in order to remove any lasting effects confounding the subsequent diet.
Following a prescreening session in which anthropometric data will be collected, participants will commence their first dietary condition. An oral glucose tolerance test will be performed before and after the two diets to measure changes in glycaemic control/whole body insulin sensitivity. Further blood samples will be taken 24 hours and 72 hours after commencing the diets in order to observe the time course of any changes in circulating hepatokine and appetite hormone concentrations. Physical activity will also be monitored for the duration of the two dietary conditions to ensure that habitual physical activity levels are maintained.
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Number of arms
- 2
- Model description
- The study design is a randomised, controlled, crossover design in which participants undertake two 7-day dietary conditions in a randomised order with a three week washout period in between.
| Arm | Type | Receives |
|---|---|---|
| High-fat diet | Experimental | Dietary Supplement: High-fat dietParticipants will consume a hypercaloric, high-fat diet. Participants will be provided with all the food during the week and will be instructed to consume all of the foods provided and no extra calorie containing food or drink. In the event of leftover food, participants will be asked to return the food for measurement and subsequent subtraction from their total energy intake. |
| Control diet | No intervention | –Participants will consume their normal 'habitual' diet for seven days which will be compared to their habitual diet recorded by a three day food diary before commencing the two diets. Participants will be instructed to carry on as normal and eat their usual diet and this period will be used as a comparator to the high-fat diet. They will also be told to record their food intake for 3 days during the diet to quantify their control diet. |
Who may qualify
- Ages
- 18 to 40 years
- Sex
- Male only
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (7 listed)
- Recreationally active - ≤ 2 structured exercise sessions per week
- BMI between 18.5 - 27.9 kg/m2
- Body fat percentage < 20%
- Metabolically healthy - No known cardiovascular or metabolic disease such as diabetes, respiratory or heart disease.
- Non-smoker
Key exclusion criteria (2 listed)
- Contraindications to exercise
- Needle Phobia
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 |
|---|---|---|
| High-fat dietThe high-fat diet will provide 7 days of overfeeding comprising of: +50% extra calories above the daily required intake, 65% of which is fat. | Dietary supplement | High-fat diet |
Primary outcome
Leukocyte cell-derived chemotaxin 2 (LECT2)
Time frame: Baseline, 1 day, 3 days, 7 days
Time-course of LECT2 plasma concentrations across the 7-day dietary interventions
17 secondary outcomes
Fibroblast growth factor 21 (FGF21)
Time frame: Baseline, 1 day, 3 days, 7 days
Fetuin-A
Time frame: Baseline, 1 day, 3 days, 7 days
Acylated ghrelin
Time frame: Baseline, 1 day, 3 days, 7 days
Peptide YY (PYY)
Time frame: Baseline, 1 day, 3 days, 7 days
C-Terminal Telopeptide of Type 1 Collagen (CTX)
Time frame: Baseline, 1 day, 3 days, 7 days
N-Terminal Propeptide of Type 1 Procollagen (P1NP)
Time frame: Baseline, 1 day, 3 days, 7 days
Visual Analogue Scale for Subjective Ratings of Appetite
Time frame: Baseline, 1 day, 3 days, 7 days
Subjective food preference
Time frame: Baseline, 1 day, 3 days, 7 days
Whole-body insulin sensitivity
Time frame: Baseline, 7 Days
Homeostasis model assessment of insulin resistance (HOMA-IR)
Time frame: Baseline, 1 day, 3 days, 7 days
Adipose tissue insulin resistance (ADIPO-IR)
Time frame: Baseline, 1 day, 3 days, 7 days
Physical activity and sedentary behaviour
Time frame: 7 days (per diet)
Resting Metabolic Rate
Time frame: Baseline, 7 Days
Fat Oxidation
Time frame: Baseline, 7 Days
Blood pressure
Time frame: Baseline, 1 day, 3 days, 7 days
Body weight
Time frame: Baseline, 1 day, 3 days, 7 days
Body fat percentage
Time frame: Baseline, 7 Days
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 18 Feb 2019.
- Background: PubMed 17550778Badman MK, Pissios P, Kennedy AR, Koukos G, Flier JS, Maratos-Flier E. Hepatic fibroblast growth factor 21 is regulated by PPARalpha and is a key mediator of hepatic lipid metabolism in ketotic states. Cell Metab. 2007 Jun;5(6):426-37. doi: 10.1016/j.cmet.2007.05.002.
- Background: PubMed 20482516Dasgupta S, Bhattacharya S, Biswas A, Majumdar SS, Mukhopadhyay S, Ray S, Bhattacharya S. NF-kappaB mediates lipid-induced fetuin-A expression in hepatocytes that impairs adipocyte function effecting insulin resistance. Biochem J. 2010 Aug 1;429(3):451-62. doi: 10.1042/BJ20100330.
- Background: PubMed 11220283Groop LC. Insulin resistance: the fundamental trigger of type 2 diabetes. Diabetes Obes Metab. 1999 May;1 Suppl 1:S1-7. doi: 10.1046/j.1463-1326.1999.0010s1001.x.
- Background: PubMed 25630516Hulston CJ, Churnside AA, Venables MC. Probiotic supplementation prevents high-fat, overfeeding-induced insulin resistance in human subjects. Br J Nutr. 2015 Feb 28;113(4):596-602. doi: 10.1017/S0007114514004097. Epub 2015 Jan 29.
- Background: PubMed 24478397Lan F, Misu H, Chikamoto K, Takayama H, Kikuchi A, Mohri K, Takata N, Hayashi H, Matsuzawa-Nagata N, Takeshita Y, Noda H, Matsumoto Y, Ota T, Nagano T, Nakagen M, Miyamoto K, Takatsuki K, Seo T, Iwayama K, Tokuyama K, Matsugo S, Tang H, Saito Y, Yamagoe S, Kaneko S, Takamura T. LECT2 functions as a hepatokine that links obesity to skeletal muscle insulin resistance. Diabetes. 2014 May;63(5):1649-64. doi: 10.2337/db13-0728. Epub 2014 Jan 29.
- Background: PubMed 28621339Meex RCR, Watt MJ. Hepatokines: linking nonalcoholic fatty liver disease and insulin resistance. Nat Rev Endocrinol. 2017 Sep;13(9):509-520. doi: 10.1038/nrendo.2017.56. Epub 2017 Jun 9.
- Background: PubMed 28115026Parry SA, Smith JR, Corbett TR, Woods RM, Hulston CJ. Short-term, high-fat overfeeding impairs glycaemic control but does not alter gut hormone responses to a mixed meal tolerance test in healthy, normal-weight individuals. Br J Nutr. 2017 Jan;117(1):48-55. doi: 10.1017/S0007114516004475. Epub 2017 Jan 24.
- Background: PubMed 21829679Uebanso T, Taketani Y, Yamamoto H, Amo K, Ominami H, Arai H, Takei Y, Masuda M, Tanimura A, Harada N, Yamanaka-Okumura H, Takeda E. Paradoxical regulation of human FGF21 by both fasting and feeding signals: is FGF21 a nutritional adaptation factor? PLoS One. 2011;6(8):e22976. doi: 10.1371/journal.pone.0022976. Epub 2011 Aug 1.
- Background: PubMed 26499438Lean ME, Malkova D. Altered gut and adipose tissue hormones in overweight and obese individuals: cause or consequence? Int J Obes (Lond). 2016 Apr;40(4):622-32. doi: 10.1038/ijo.2015.220. Epub 2015 Oct 26.
- Derived from this study: PubMed 31919514Willis SA, Sargeant JA, Yates T, Takamura T, Takayama H, Gupta V, Brittain E, Crawford J, Parry SA, Thackray AE, Varela-Mato V, Stensel DJ, Woods RM, Hulston CJ, Aithal GP, King JA. Acute Hyperenergetic, High-Fat Feeding Increases Circulating FGF21, LECT2, and Fetuin-A in Healthy Men. J Nutr. 2020 May 1;150(5):1076-1085. doi: 10.1093/jn/nxz333.
- Individual participant dataSharing planned: Undecided
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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.
James A King, PhD principal investigator
Loughborough University
Scott A Willis, MSc principal investigator
Loughborough University
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing High-fat diet in people with Insulin Resistance and Type2 Diabetes Mellitus, run by Loughborough University at 2 sites in United Kingdom.
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 7 inclusion and 2 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 18 Feb 2019. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites in United Kingdom. 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?
Leukocyte cell-derived chemotaxin 2 (LECT2) (time frame: Baseline, 1 day, 3 days, 7 days). 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 NCT03369145, which also lists 10 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 18 Feb 2019.