Impaired glucose metabolism in Japanese patients with acromegaly is restored after successful pituitary surgery if pancreatic β-cell function is preserved

Abstract

Objective: Impaired glucose metabolism is common in acromegaly, but it is not clear how glucose metabolism is impaired or what predicts its restoration after cure of the disease. To identify factors involved in the impairment of glucose metabolism in acromegaly, we evaluated clinical parameters before and immediately after surgical cure of the disease. Design and methods: We retrospectively analyzed clinical data of 92 consecutive Japanese patients with acromegaly who underwent successful pituitary surgery. Patients who had received medical therapy for acromegaly or insulin treatment for diabetes were excluded. We evaluated insulin resistance (IR) and pancreatic b-cell function in addition to GH and IGF1 levels before and after surgery. Results: In this study of Japanese patients with acromegaly, average body mass index (BMI) was 23.4, and no patient had a BMIO30. IR was involved in the impairment of glucose metabolism, which was restored upon surgical cure of acromegaly if b-cell function was preserved. Insufficient b-cell function did not improve after normalization of GH/IGF1 and was associated with impaired glucose metabolism before and after surgery. Results of receiver operating characteristic analysis of preoperative clinical parameters suggest that insulinogenic index (IGI) O0.50 best predicts restoration of normal glucose metabolism upon cure of acromegaly in Japanese patients. Conclusions: IR impairs glucose metabolism in acromegaly. Once b-cell function is impaired, abnormal glucose metabolism persists even after cure of acromegaly. IGIO0.50 indicates that b-cell function is preserved in non-obese Japanese patients with acromegaly.

Ketoacidosis as the initial clinical condition in nine patients with acromegaly: a review of 860 cases at a single institute

“…Further, HOMA-%b, which is an index of basal insulin secretion, was 80G46 after surgery in patients with histories of ketoacidosis. Both parameters were similar to those observed in postsurgical acromegaly subjects who had impaired glucose metabolism before surgery and normalized glucose metabolism following complete pituitary adenomectomy (33). Thus, intrinsic insulin secretion in the patients presented here seemed to be preserved after surgery.…”

“…As we reported previously (33), normal glucose metabolism was restored in a subset of patients who underwent surgery for acromegaly. In that report (33), we divided acromegaly patients into three groups according to their glucose tolerance before and after surgery.…”

“…As we reported, acromegaly exacerbates insulin resistance. However, some patients could not secrete sufficient insulin to overcome resistance (33). High plasma levels of glucose may reduce insulin secretion from b-cells, producing glucose toxicity.…”

The Ability of β-Cells to Compensate for Insulin Resistance is Restored with a Reduction in Excess Growth Hormone in Korean Acromegalic Patients

“…It has been suggested that impaired glucose metabolism is mediated by growth hormone (GH)-induced insulin resistance. Several studies have suggested that insulin resistance contributes to abnormal glucose tolerance in acromegalic patients (6-8), but Kasayama et al (9) reported that impaired β-cell function is important in determining the glucose tolerance status in acromegalic patients, and Kinoshita et al (10) reported that once β-cell function is impaired, abnormal glucose metabolism persists even after patients have been cured of acromegaly. Therefore, both insulin resistance and pancreatic β-cell dysfunction appear to be involved in the pathogenesis of glucose homeostasis abnormalities in acromegalic patients.…”

Glucose Tolerance is Improved Following Surgery for Silent Somatotroph Adenoma

“…If the compensatory hyperfunction of pancreatic β-cells does not counterbalance the reduced insulin sensitivity, abnormal glucose tolerance is likely to become clinically evident [18]. Kinoshita et al [19] reported that abnormal glucose tolerance fails to normalize after acromegaly has been cured once the function of the pancreatic β-cells has been impaired. In the present case, the insulinogenic index suggested that the impairment in insulin secretion persisted after surgery.…”