New insights into sympathetic regulation of glucose and fat metabolism - Nonogaki (2000)
The sympathetic nervous system increases blood glucose through direct nerve stimulation of the liver
The sympathetic nervous system also increases blood glucose indirectly through the hormone epinephrine
The sympathetic nervous system inhibits insulin secretion from the pancreas
The Breathing Diabetic Summary
This article focused largely on leptin, but also provided a lot of good general information on how the sympathetic nervous system impacts blood glucose and insulin secretion. So my review will focus on these aspects and how they are related to our breathing and our diabetes.
To begin, did you know that the pancreas is supplied nerves from both the sympathetic and parasympathetic nervous systems? The sympathetic nerves increase glucagon production from the pancreas. In addition, activation of the sympathetic nerves prevents insulin secretion from the pancreas. The parasympathetic nerves, on the other hand, increase insulin secretion. From this information alone, we can see the usefulness of activating the parasympathetic nervous system, especially for type II diabetics who still produce insulin. And, we know slow breathing is an easy way to do this.
For us type I diabetics, there are additional benefits to shifting out of a sympathetic state and into a parasympathetic one. The liver also is supplied with nerves from both the sympathetic and parasympathetic nervous systems. When the sympathetic nerves are activated, the liver generates glucose. This also occurs through the hormonal effects of epinephrine (adrenaline). Thus, the sympathetic nervous system increases the body’s production of glucose both directly (through the nerves) and indirectly (through hormones released during activation). In addition to increasing blood sugar, epinephrine also contributes to insulin resistance. And, these sympathetic effects will always outweigh the parasympathetic effects. This makes sense: the sympathetic nervous system (fight or flight) is there to save your life, and therefore it has priority. However, we know from previous studies that diabetics spend too much time in a sympathetic state. We also know that people who naturally breathe faster have higher levels of sympathetic activation. Fortunately, we can use light, slow breathing to consciously shift ourselves into a parasympathetic state to offset this imbalance.
As a side note, holding your breath activates the sympathetic nervous system, which might sound like a bad idea after reading the previous two paragraphs. However, we use breath holds to activate the sympathetic nervous system deliberately, intermittently, and with control so that we can reap the many benefits associated with hypoxia.
Overall, this paper shows us that the sympathetic nervous system increases blood glucose concentrations by increasing the liver’s production of glucose via direct nerve stimulation and hormonal effects from epinephrine. This paper was packed full of other information on the nervous system and leptin, and I didn’t even scratch the surface here. But, for us, the take home message is that reducing our sympathetic activity will help us reduce our blood sugars. And the easiest way to do this is through slow breathing.
Abstract from Paper
The autonomic nervous system modulates glucose and fat metabolism through both direct neural effects and hormonal effects. This review presents recent concepts on the sympathetic regulation of glucose and fat metabolism. Focally released norepinephrine from sympathetic nerves is likely to increase glucose uptake in skeletal muscle and adipose tissues independent of insulin but norepinephrine does not contribute so much as epinephrine to hepatic glucose production. Epinephrine increases hepatic glucose production and inhibits insulin secretion and the glucose uptake by tissues that is induced by insulin. Additionally, catecholamines can increase thermogenesis and lipolysis, leading to increased energy expenditure and decreased fat stores. It is likely that b-(b3)- adrenergic receptors mediate these responses. Alterations of central neurotransmission and environmental factors can change the relative contribution of sympathetic outflow to the pancreas, liver, adrenal medulla and adipose tissues, leading to the modulation of glucose and fat metabolism. Recent studies have proposed that leptin, an adipocyte hormone, affects the central nervous system to increase sympathetic outflow independent of feeding. The effects of leptin on glucose and fat metabolism could be in part mediated by the sympathetic nervous system. Studies using mice with a genetic disruption of serotonin 5-HT2c receptor indicate that central neural mechanisms in the regulation of sympathetic outflow and satiety could be dissociated. Abnormalities of sympathetic effects, including disturbances of leptin and b3-adrenergic receptor signalling, are likely to cause obesity and impaired glucose tolerance in rodents and humans. These findings indicate that dysfunction of the sympathetic nervous system could predispose to obesity and Type II (non-insulin-dependent) diabetes mellitus.
K.Nonogaki, (2000) New insights into sympathetic regulation of glucose and fat metabolism, Diabetologia, 43, 533-549.