{"id":19253,"date":"2024-11-18T14:23:08","date_gmt":"2024-11-18T19:23:08","guid":{"rendered":"https:\/\/foodmedcenter.org\/?p=19253"},"modified":"2024-11-18T18:38:20","modified_gmt":"2024-11-18T23:38:20","slug":"study-spotlight-take-away-with-chef-dr-mike-diabetes-and-stress-eating","status":"publish","type":"post","link":"https:\/\/foodmedcenter.org\/zh_cn\/study-spotlight-take-away-with-chef-dr-mike-diabetes-and-stress-eating\/","title":{"rendered":"Study Spotlight Take-Away with Chef Dr. Mike: Diabetes and stress eating"},"content":{"rendered":"
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\u201cIt\u2019s not stress that kills us; it is our reaction to it.\u201d<\/em><\/p>\n\n\n\n

\u2014 Hans Selye<\/em><\/p>\n<\/blockquote>\n\n\n\n

In his book, The Stress of Life<\/em>, published in 1956, physician and researcher Hans Selye opened the door to understanding the relationship between stress and its effects on the human body and mind. Stress comes in many forms, and human beings who are subjected to it manifest it in a myriad of ways. Last week\u2019s Study Spotlight<\/a> examined the effects of chronic continuous low-level inflammation on the gut microbiome and its possible contribution to the risk of developing Alzheimer\u2019s-type dementia later in life.<\/p>\n\n\n\n

Such chronic, continuous, low-level inflammation is also a hallmark of obesity and type II diabetes mellitus. Though often characterized by BMI alone, the pathophysiology of true obesity (not just being overweight) involves a hyperreactive inflammatory response. This imbalance of normal immune function may be one reason that obesity is associated with an increased risk of developing type 2 diabetes. The risk of developing diabetes is over 3-fold higher in overweight individuals and more than 10-fold higher in obese individuals compared with lean individuals.<\/p>\n\n\n\n

Obesity appears to lead to the development of type II diabetes through the induction of insulin resistance. Insulin resistance can result in fat cell dysfunction. A consequence is the growth of the adipose cells and increased adipose tissue inflammation and fibrosis. This can affect the liver, leading to unrestrained hepatic glucose production (hGP), which is a key driver of fasting hyperglycemia in diabetes. Such liver involvement is also believed to contribute to hepatic steatosis that can progress to metabolic dysfunction-associated fatty liver disease (MAFLD). MAFLD is present in more than 70% of people with type 2 diabetes and is the most common reason for fibrosis and liver failure.<\/p>\n\n\n\n

However, exactly how this occurs remains poorly understood. It is generally thought impaired cellular insulin signaling is the primary driver of insulin resistance. However, this week\u2019s study suggests that overeating (overnutrition) increases the stress hormone norepinephrine. This, in turn, causes increased activity of the sympathetic nervous system (SNS). Using a mouse model, researchers demonstrated that reducing catecholamine (CA, e.g., norepinephrine) release from the SNS protects against overnutrition-induced insulin resistance and hyperglucagonemia, adipose tissue dysfunction, and fatty liver disease. This suggests that \u201cA key mechanism through which heightened sympathetic nervous system activity (SNA) induces insulin resistance is by triggering adipose tissue lipolysis. Increased SNA emerges as a critical driver in the pathogenesis of overnutrition-induced insulin resistance and metabolic disease independent of cellular insulin signaling.\u201d In other words, it may be over-activation of the sympathetic nervous system, responsible for the flight, fight, or freeze response, associated with overeating that paves the way for the development of obesity and obesity-related type II diabetes.<\/p>\n\n\n\n

The Study:<\/a><\/p>\n\n\n\n