Obesity is an important risk factor for osteoporosis and fractures. With the growing prevalence of obesity in the U.S., understanding the pathophysiology of bone loss in this population is of importance to public health. Growth hormone (GH) is a critical mediator of bone homeostasis and is markedly reduced in obesity. Our preliminary data suggest an important role for the GH/insulin-like growth factor 1 (IGF-1) system in the pathogenesis of bone loss in obesity. The development of novel imaging techniques provides an opportunity to investigate the effects of GH on skeletal structure and strength, which will provide insights into the pathogenesis of obesity related bone loss. Understanding the pathophysiology of bone loss in obesity may help identify new treatment targets for this important complication. The investigator hypothesizes that low-dose GH administration for 18 months will improve skeletal health.

Inclusion Criteria:

• Ages 18-65 and generally healthy
• BMI ≥ 25 kg/m2
• Bone mineral density (BMD) T score ≤ -1.0 and > -2.5 (as measured by DXA)

Exclusion Criteria:

• For women: amenorrhea for 3 months, pregnancy or breastfeeding, polycystic ovary syndrome
• History of diabetes mellitus, cancer or other serious chronic disease
• Use of osteoporosis medications
• Anemia

18 months

Growth hormone (Pfizer) is FDA approved and has a possible side-effect profile described/listed in the medication package insert. The investigators recorded all adverse events (as defined by the clinicaltrials.gov definition) and categorized them by "expected" (eg listed in the medication package insert) and "unexpected" (not listed in the medication package insert).

# of events = # of subjects that experienced the side effect at any point during the study.

Study medication was discontinued at 18 months. Subjects were followed for an additional 6 months off of study medication. The data reported here are for the primary 18-month trial.