Adipose Tissue and Serum Inflammation in Growth Hormone (GH) Deficiency
Trial Snapshot
- Phase
- Not Applicable
- Status
- Completed
- Sponsor
- Columbia University
- Enrollment
- 19
- Locations
- 1
- Primary Endpoint
- Visceral Adipose Tissue (VAT) mass
Study Overview
Brief Summary
This study will examine adipose tissue inflammation and adipokine expression and serum markers of inflammation and adipokine levels in patients with growth hormone (GH) deficiency before and after treatment.
Detailed Description
The GH axis has important influences on adipose tissue. Preliminary data from the investigators' study in acromegaly, a state of GH excess, suggests that GH reduces adipose tissue (AT) mass and serum inflammation. However, GH seems to reduce macrophage markers in adipose tissue yet increase adipocyte inflammation. This novel dissociation of macrophage and adipocyte inflammation is hypothesized to be due to GH. In order to examine this hypothesis further this study will examine adipose tissue and serum inflammation in patients with GH deficiency before and after GH therapy. The investigators will obtain subcutaneous adipose tissue by biopsy in patients with active GH deficiency planning to undergo therapy for GH deficiency. Concurrently serum samples will be taken for analysis of levels of inflammatory markers and adipokines. After treatment for 12 months with a normal levels of Insulin-like growth factor 1 (IGF-1), a marker of GH deficiency, patients will have a repeat adipose tissue biopsy. Adipose tissue parameters will be analyzed in each specimen and then compared to each patient over time as well as to body mass index (BMI)-matched control subjects.
Study Design
- Study Type
- Observational
- Observational Model
- Cohort
- Time Perspective
- Prospective
Eligibility Criteria
- Ages
- 18 Years to 65 Years (Adult, Older Adult)
- Sex
- All
- Accepts Healthy Volunteers
- No
Inclusion Criteria
- Not provided
Exclusion Criteria
- •Have other conditions that may result in abnormal GH and/or IGF-I concentrations (e.g., severe hepatic disease, severe renal disease, malnutrition, treatment with levodopa).
- •Alanine aminotransferase (ALT) or aspartate transaminase (AST) ≥ 2 x upper limit of normal or clinically significant hepatic disease or renal impairment defined as creatinine > 1.5x upper normal.
- •Have a pituitary adenoma with a distance to the optic chiasm of 5 mm or less, confirmed by a recent MRI scan (within two months prior to the screening visit).
- •Pituitary tumor growth within the 12 months prior to study entry.
- •GH therapy within 6 months of screening.
- •Diabetes mellitus.
- •History of acromegaly.
- •History of active Cushing's disease within 24 months of screening
- •Visual field defects or other neurological symptoms due to current tumor mass compression.
- •Have known or suspected drug or alcohol abuse.
- •Have received an investigational medication within four weeks prior to Screening or is scheduled to receive any investigational medication during the study.
- •Do not have the ability to fully comprehend the nature of the study, to follow instructions, cooperate with study procedures, and/or are unable to adhere to the visit scheduled outlined in the protocol.
- •Have other severe acute or chronic medical or psychiatric condition or laboratory abnormality that may increase the risk associated with study participation or study drug administration or may interfere with the interpretation of study results and, in the judgment of the investigator, would make the subject inappropriate for entry into this study.
- •History of a malignancy other than squamous or basal cell skin carcinoma that has been excised or intracranial malignant tumors or leukemia within 5 years of screening.
- •Patients who have a known hypersensitivity to growth hormone therapy
- •Use of weight 349 loss medications
- •Females who plan to change estrogen therapy during the trial
- •Patients who have received supraphysiologic doses of glucocorticoids within the past 6 months (except for peri-operative (< 3 days duration) of dexamethasone), or who are currently receiving any chemotherapeutic agents.
- •Patients who have received other investigational drugs administered or received within 30 days of study entry
Arms & Interventions
Adults with growth hormone deficiency
Subjects who present to the neuroendocrine unit at Columbia University Irving Medical Center (CUIMC) for therapy of GH deficiency or who are followed in the unit and have active GH deficiency and are planning to initiate a therapy.
Intervention: Growth Hormone (Drug)
Outcomes
Primary Outcomes
Visceral Adipose Tissue (VAT) mass
Time Frame: Baseline to 12 months of GH therapy
Visceral adipose tissue mass as measured by tota body magnetic resonance imaging
Secondary Outcomes
- Relative gene expression values of MCP1 gene(Baseline to 12 months of GH therapy)
- Total body fat(Baseline to 12 months of GH therapy)
- Relative gene expression IL6 gene(Baseline to after 12 months of treatment for GH deficiency)
- Relative gene expression of CD68 gene(Baseline to 12 months of GH therapy)
- TNFα level(Baseline to 12 months of GH therapy)
- Intra-hepatic lipid level(Baseline to 12 months of GH therapy)
- Skeletal Muscle Mass(Baseline to 12 months of GH therapy)
- Resting metabolic rate(Baseline to 12 months of GH therapy)
- homocysteine level(Baseline to 12 months of GH therapy)
- Relative gene expression values of CD11c gene(Baseline to 12 months of GH therapy)
- interleukin 6 (IL-6) level(Baseline to 12 months of GH therapy)
- CRP level(Baseline to 12 months of GH therapy)
Investigators
Pamela U. Freda
Professor of Medicine
Columbia University