Liraglutide as a potentially useful agent in regulating appetite in diabetic patients with hypothalamic-pituitary disorders

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 142-166-Hypothalamus-Pituitary Development & Biology
Basic/Clinical
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-155
Ai Haraguchi*, Haruko Takashima, Shoko Natsuda, Takao Ando, Norio Abiru, Hironori Yamasaki and Atsushi Kawakami
Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
Background: GLP-1 analogues are known to improve diabetes mellitus (DM) partially through their effect of suppressing appetite. It is believed that anorexia associated with GLP-1 analogue treatment is at least partially mediated by direct activation of the GLP-1 receptor in the central nervous system via peripherally administered GLP-1 analogues. We report on three diabetic patients in whom the GLP-1 analogue liraglutide (L) was highly effective in suppressing appetite.

Clinical cases

Case 1: A 77-year-old man was diagnosed with panhypopituitarism and central diabetes inspidus (DI) putatively caused by IgG4-related pituitary disease.  He was thereafter treated with deficient hormones including testosterone (T) and growth hormone (GH). However, he developed prostate cancer one year after initiating T and GH therapy, and thus these hormones were discontinued. He then complained of severe fatigue and 2 kg of weight gain, and soon developed DM, with his HbA1c increasing from 5.6% to 9.5%. His DM has been successfully treated with 15 mg of pioglitazone and 0.3 mg of L. Although his body weight increased 6 kg after L was started, his DM remained well controlled. Of note, the patient complained of severe appetite loss upon increasing the dose of L from 0.3mg to 0.6mg.

Case 2: A 70-year-old man was diagnosed with panhypopituitarism and central DI, which  developed after aseptic meningitis that was likely related to treatment of cerebral artery aneurysm. After initiating glucocorticoid treatment, his appetite increased and he gained 3 kg over two months. The patient soon developed DM. His DM has been successfully treated with 0.3 mg of L. The patient complained of severe appetite loss upon increasing the dose of L from 0.3 mg to 0.6 mg. He did not gain weight thereafter.

Case 3: A 38-year-old man with adult GH deficiency and central DI, caused by traumatic brain injury at age 17, was treated with DDAVP and GH. He also developed DM at age 23, and was being treated with 1 mg of glimepiride and 750 mg of metformin. However, because of frequent overeating and consequent weight gain, his DM was poorly controlled. After introducing L, his appetite declined and he stopped gaining weight. His DM has been well controlled with 0.9 mg of L, with HbA1c levels at approximately 6.5%.

Conclusion: The GLP-1 analogue, L, was highly effective in regulating appetite and improving DM in these three cases. More importantly, beneficial effects were seen with small doses of L in two of the cases. We hypothesize that L might have better access to the GLP-1 receptor in the central nervous system, possibly due to the partial disruption of the blood-brain barrier associated with the underlying hypothalamic-pituitary disorders in these patients. Our findings indicate that there may be potential benefit in using GLP-1 analogues to regulate appetite in patients with hypothalamic-pituitary disorders.

Nothing to Disclose: AH, HT, SN, TA, NA, HY, AK

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