Mood state as a blood glucose modulator in a patient with bipolar disorder and diabetes mellitus: A case report

To the Editor

We present a case of a 59-year-old Taiwanese male with bipolar disorder and type 2 diabetes mellitus (DM) for about 10 years, both untreated for the most recent 3 years. In September 2016, he visited our institute due to a depressive episode. The laboratory examinations revealed elevated glycated hemoglobin A1 (HbA1c) 12.4% (reference: 4–6.5%). He received psychotropic and antidiabetic drugs for 2 months. His mood became stable, and his blood glucose level (BGL) normalized with HbA1c 6.2%. Then, he stopped his antidiabetic drugs due to normalized BGL (71 mg/dL, reference: 70–126 mg/dL). In the following months, he displayed hyperthymia.

During January to April 2017, the patient experienced a manic episode. Although he did not take any antidiabetic drugs for more than 3 months, his DM was still well managed (HbA1c: 5.7% in March 2017). In May 2017, another depressive episode occurred. Two months later, his HbA1c increased to 8.1%, and the fasting BGL was 145 mg/dL, representing a relapse of DM. The patient had no other medical abnormalities, and his body weight and diet showed no obvious changes. The patient’s clinical manifestations and medications are illustrated in Figure 1. His caregiver confirmed that the patient had good adherence to the psychotropic drugs, which may impact on glycemic control and HbA1c.

Figure 1.

The patient’s medications and the clinical manifestations.

Because peripheral dopamine may elevate during manic phases and decrease during depressive phases, the homeostatic function of circulating dopamine may moderate BGL in the following ways (Hochman et al., 2014): first, the increased peripheral dopamine may stimulate cardiac contractility and vasodilation and induce diuresis and natriuresis, leading to relative hemodilution in manic phases and relative hemoconcentration in depressive phases; our patient had consistent findings (Figure 1). Then, relative hemodilution could cause less secretion of vasopressin, a hormone that decreases body fluid tonicity; therefore, reduced level of vasopressin may lead to less activity of hypothalamic-pituitary-adrenal axis by less stimulation of relevant receptors, resulting in a decrease in hepatic glyconeogenesis and BGL (Nakamura et al., 2017). Besides serum osmolality alternation, evidence suggests that reduced circulating dopamine can cause serum glucose metabolism impairment (Pérez-Cornago et al., 2014); therefore, the author theorized that dopamine has a key role in carbohydrate metabolism.

Evidence has implied an imbalance of fluid and electrolyte homeostasis in episodes of bipolar disorder. Our case suggests that the link between mood switching and fluid homeostasis may lead to DM moderation. Future studies are encouraged to validate our findings.