Serum Betatrophin Levels and Its Influencing Factors in Patients With Hyperthyroidism

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Total Enrollment

240 participants

Study Classification

OBSERVATIONAL

Study Start Date

2016-07-31

Study Completion Date

2017-06-30

Brief Summary

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Clustering of various metabolic parameters including abdominal obesity, hyperglycaemia, low high-density lipoprotein cholesterol, elevated triglycerides and hypertension have been used worldwide as metabolic syndrome to predict cardiometabolic risk. Thyroid dysfunction impacts on various levels of these components.

Recent evidence from HepG2 cells indicates that betatrophin, also known as TD26/RIFL/lipasin/ANGPTL8/C19orf80, a secreted protein that regulates glucose, lipid metabolism, and energy homeostasis, is induced by T3. However, the role of betatrophin in hyperthyroid patients is unknown.

The objective was to study serum betatrophin levels in hyperthyroid patients and the association of serum betatrophin levels with hyperthyroidism.

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Detailed Description

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Thyroid hormone (TH) is a critical hormone responsible for growth, development, and metabolism. It maintains basal metabolic rate (BMR), improves adaptive thermogenesis, and thus modulates body weight by fine-tuning energy expenditure and intake. Hyperthyroidism, a condition with excess TH, presents a status of negative energy balance that is characterized by weight loss, increased energy expenditure, and accelerated lipolysis and gluconeogenesis. The mechanism underlying hypermetabolic status in hyperthyroidism is complicated. In hyperthyroidism, excess TH promotes the metabolism rate primarily by binding to TH receptor α or β, and in turn by further influencing diverse metabolic pathways. Recent studies have revealed that TH signals were involved in cross talk with a range of other metabolic signaling pathways in different metabolic organs. In liver, TH interacts with peroxisome proliferator-activated receptor (PPAR) α, PPARγ, and liver X receptor α pathway; promotes fatty acid oxidation; decreases cholesterol; and enhances gluconeogenesis. The elements required for TH action are well documented, but understanding the interaction between TH and various pathways remains a challenge.

Betatrophin, also known as TD26/RIFL/lipasin/ANGPTL8/C19orf80, is a novel protein predominantly expressed in human liver. Increasing evidence has revealed associations between betatrophin expression, glycemia and serum lipid profiles, particularly in patients with obesity or diabetes. Stimulators of betatrophin, such as insulin, thyroid hormone, irisin, SIRT1 and caloric intake, are usually relevant to energy expenditure or thermogenesis. A previous report revealed that betatrophin mRNA is induced by the thyroid hormone in HepG2 cells. Subsequent studies confirmed that transcriptional regulation is dependent on the thyroid hormone receptor that binds to the betatrophin upstream element. Therefore, betatrophin is a novel gene dramatically activated by the thyroid hormone. However, there is no evidence to date showing that TH is capable of regulating betatrophin expression in human beings. The current study investigated the change of betatrophin levels in patients with hyperthyroidism before and after thionamide treatment and explored the association of serum betatrophin levels with hyperthyroidism.

Conditions

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Hyperthyroidism

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

CROSS_SECTIONAL

Study Groups

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Hyperthyroid Patients

Patients with hyperthyroidism

thionamide treatment for 3 months

Intervention Type DRUG

Hyperthyroid patients would received thionamide treatment (methimazole, propylthiouracil, or propranolol) for 3 months, and euthyroidism would be obtained.

NC group

Normal control subjects

No interventions assigned to this group

Interventions

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thionamide treatment for 3 months

Hyperthyroid patients would received thionamide treatment (methimazole, propylthiouracil, or propranolol) for 3 months, and euthyroidism would be obtained.

Intervention Type DRUG

Other Intervention Names

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methimazole, propylthiouracil, or propranolol

Eligibility Criteria

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Inclusion Criteria

* Clinical diagnosis of hyperthyroidism
* Must be drug-naive before recruitment

Exclusion Criteria

* diabetes
* hypertension
* cancer
* pregnancy
* lactation
* subacute thyroiditis
* postpartum thyroiditis
* abnormal liver function
* abnormal kidney function
* infectious diseases

Minimum Eligible Age

18 Years

Maximum Eligible Age

60 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Responsible Party

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Hu Hao

Deputy Director, Department of endocrinology, Principal Investigator, Clinical Associate Professor

Responsibility Role SPONSOR_INVESTIGATOR