April 26, 2017
Dynamic Duo: Blood Sugar
& Neurotransmitter Secretion

In patients with insulin resistance and or metabolic syndrome, salivary testing typically uncovers hormone imbalance. In females, elevations of androgens and perhaps a corresponding increase in estradiol is observed, and in males, a decrease in testosterone (and perhaps a corresponding increase in estradiol) is observed. While balancing hormones can be extremely beneficial and necessary to help restore equilibrium within a patient’s unique physiology and can lead to an improved quality of life, the reality is that some conditions, such as metabolic syndrome in and of itself can also create neurotransmitter imbalance.

Metabolic syndrome can be classified as a state of sympathetic nerve hyperactivity. Typically, this state is associated with elevations in norepinephrine (NE) and epinephrine, with the majority of increase seen in NE. De Pergolal et. al examined this phenomenon and has suggested that insulin and NE work independently, yet together in the development of metabolic syndrome. This study examined a population of healthy euthyroid overweight and obese subjects to understand this relationship. The results showed a significant relationship between metabolic syndrome and elevations of both insulin and NE levels independent of age, sex, TSH, thyroid hormones, and epinephrine levels. Additionally, this study points to insulin as a determinant for alterations in metabolic aspects while NE appear to be more important in the development of hypertension and impaired glucose metabolism.

Additionally, multifactorial health problems such as Polycystic Ovarian syndrome (PCOS) or diabetes, which also share an insulin resistance and/or metabolic syndrome component, can show an imbalance in neurotransmitter levels. As discussed previously, the increased sympathetic activity seen in PCOS can lead to an increase in NE. In addition to NE, GABA may also play a role in PCOS as well as type 2 diabetes when examining the insulin resistant aspects of these disease processes.

Recent studies have demonstrated in addition to insulin, GABA can be produced by β-cells of the pancreases where it functions as an intraislet transmitter regulating islet cell secretion and function. In a review article by Wan et. al., several rodent studies as well as in vivo studies of xenotransplanted human islet cells, show GABA appears to have β-cell regenerative properties and may protect these cells against apoptosis induced by cytokines, drugs, and other stressors. Interestingly, when utilized as a potential treatment for diabetes, “oral GABA treatment increased graft-cell proliferation and decreased apoptosis, leading to a significantly enhanced β-cell mass. Furthermore, GABA lowered blood glucose levels and ameliorated glucose tolerance.”

Research focused on Type 1 diabetes has shown a higher incidence of depression. One study looked at 19 adults who were not depressed; eight with type 1 diabetes and 11 healthy controls. Using MRI to measure brain activity and magnetic resonance spectoroscopy to measure the level of glutamate, subjects underwent these scans when their blood sugar level was normal (90-110mg/dL) and also after a continuous infusion of glucose, which moderately raised their glucose (180 to 200mg/dL). The results showed acutely raising blood glucose level also elevated glutamate in the area of the brain responsible for controlling emotions in the type 1 diabetes subjects, but not in controls. While further exploration is needed to definitively explain the role specific neurotransmitters play in the pathogenesis of diseases like insulin, resistance, diabetes, and metabolic syndrome, neurotransmitter levels throughout the body have an influence in the progression as well as the potential for regression of disease processes.

References:
  • De Pergola G, Giorgino F, Benigno R. Independent influence of insulin, catecholamines, and thyroid hormones on metabolic syndrome. Obesity (Silver Spring). 2004;16(11):2405-2411. doi:10.1038/oby.
  • Wang Q, Prud'homme G, Wan Y. GABAergic system in the endocrine pancreas: a new target for diabetes treatment. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. February 2015:79-87. doi:10.2147/dmso.s50642.
  • Endocrine Society. "High blood sugar causes brain changes that raise depression risk." ScienceDaily. ScienceDaily, 23 June 2014. releases/2014/06/140623092011.htm>.
  • Lam RW, Levitan RD. Pathophysiology of seasonal affective disorder: a review. J Psychiatry Neurosci. 2000;25(5):469-80.
Disclaimer:

All information given about health conditions, treatment, products, and dosages are for educational purposes only and do not constitute medical advice.



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