Shortly after finishing her master\u2019s degree at Johns Hopkins University, Ana Montes was hired at the US Defense Intelligence Agency (DIA). What the DIA didn\u2019t know was that she already had been hired by the Cuban government. For 16 years she was a double agent and, in that time, did a considerable amount of damage for someone so unknown.<\/p>\n\n\n\n
The pancreas is partially composed of cells that function as insulin factories. They’re called beta cells (\u03b2 cells). While we\u2019ve been focusing on insulin resistance in our quest to better understand type-2 diabetes, we’re now going to look at how these factories get sabotaged, as this contributes to type 2 diabetes.<\/p>\n\n\n\n
\u03b2 cells produce and store insulin and another substance called amylin. \u03b2 cells also function as glucose sensors that detect rising blood sugar levels. Once they are given the heads up that blood sugar is changing, they quickly respond by releasing some of their stored insulin and amylin while simultaneously producing more. When diagnosing diabetes, the C-peptide blood test is commonly given to assess \u03b2 cells’ functionality. The functionality of \u03b2 cells is extremely important and when their work is impaired, it’s referred to as \u03b2 cell dysfunction, a defining characteristic of diabetes.<\/p>\n\n\n\n
As insulin resistance develops, \u03b2 cells churn out more insulin to compensate for higher blood sugar levels. In fact, an elevated insulin level in the blood is an early detector of insulin resistance, which can be followed, perhaps even years later, with high blood sugar levels. Another marker of early dysfunction is when \u03b2 cells don’t or can’t adequately compensate for excess nutrition or the insulin resistant state with sufficient insulin. Fasting blood sugars may be normal, but post-meal levels are elevated. The body seeks to maintain homeostasis of normal blood sugar levels as \u03b2 cells literally adapt their mass and function to meet the need. Unfortunately, \u03b2 cells’ dysfunction can progress over time, which can include loss of \u03b2 cells; impaired sensing of blood sugar levels; and poor response of \u03b2 cells to meals, which is due to altered insulin production, storage, or secretion, etc. The result is what some refer to as \u03b2 cell exhaustion. Progressive loss of beta-cell function occurs throughout the course of the disease. So, we\u2019ve got insufficient insulin to meet the demands of escalating blood sugar levels, an impaired signaling system, delayed insulin release, and reduced insulin secretion throughout the day. The result is high blood sugar levels.<\/p>\n\n\n\n
What disturbs \u03b2 cell function?<\/p>\n\n\n\n
Research has found that one of the main culprits to \u03b2 cell death and dysfunction is inflammation.<\/p><\/blockquote>\n\n\n\n
Overweight, overeating, the amount of simple carbohydrates in the diet, excess of sweet drinks, a general lack of physical activity\u2014all place a high strain on \u03b2 cell resources. Couple that with insulin resistance and the burden accelerates beta cell dysfunction. As we just learned, \u03b2 cells do their best to adapt to the situation but cannot hold out forever. There are other factors too that act as \u03b2 cell insults, weakening the pancreas\u2019s ability to handle our food intake.<\/p>\n\n\n\n
Research has found that one of the main culprits to \u03b2 cell death and dysfunction is inflammation. Our immune cells produce a family of substances called cytokines. Some of these cytokines are protective while others induce inflammation and are damaging to the \u03b2 cells. When the scale chronically tips in favor of pro-inflammatory, the over-exposure to damaging cytokines results in damage to \u03b2 cells. There are circulating cytokines produced elsewhere in the body that infiltrate the pancreas, but there are also a variety of cytokines produced in the pancreas itself. \u201cThese locally produced cytokines play important roles in regulation of pancreatic \u03b2-cell function as well. To maintain the normal pancreatic \u03b2-cell function, the deleterious and protective cytokines need to be balanced.\u201d1<\/sup> Inflammation in the pancreas is not a good thing.<\/p>\n\n\n\n
Fat in the pancreas isn’t good either. Fat can actually be stored in and around the pancreas and this fat has also been found to adversely affect \u03b2 cell function by changing how things work. In a research trial, 18 individuals with type-2 diabetes were found to have increased levels of fat in the pancreas. This intrapancreatic fat was reduced to a normal level as a result of bariatric surgery induced weight lost. The lead researcher, Professor Roy Taylor, said:<\/p>\n\n\n\n
When \u03b2 cells start dying off or start malfunctioning, we’re in the throws of diabetes.<\/p><\/blockquote>\n\n\n\n
\u201cFor people with Type 2 diabetes, losing weight allows them to drain excess fat out of the pancreas and allows function to return to normal. So if you ask how much weight you need to lose to make your diabetes go away, the answer is one gram! But that gram needs to be fat from the pancreas. At present the only way we have to achieve this is by calorie restriction by any means\u2026 This new research demonstrates that the change in level of fat in the pancreas is related to the presence of Type 2 diabetes in a patient. The decrease in pancreas fat is not simply related to the weight loss itself. It is not something that might happen to anyone whether or not they had diabetes. It is specific to Type 2 diabetes. What is interesting is that regardless of your present body weight and how you lose weight, the critical factor in reversing your Type 2 diabetes is losing that 1 gram of fat from the pancreas.\u201d2<\/sup><\/p>\n\n\n\n
Guess what that pancreatic fat can produce? Pro-inflammatory cytokines! So, let\u2019s get this straight. When \u03b2 cells start dying off or start malfunctioning, we’re in the throws of diabetes. Inflammation does its part in setting this off. Where does this inflammation come from? Potentially from several sources, but one is pancreatic fat stores. These fat cells produce cytokines that can do in-house devastation to the insulin producing factories (\u03b2 cells).<\/p>\n\n\n\n
Ana Montes did a lot of damage, handing over top US secrets to Cuba due to the fact that she was undetected for many years. Our bodies are being hijacked, and the sooner we identify what we’re really up against, the more we can do to stop the damage. This is true in the spiritual realm. Scripture lets us know that the real enemy isn\u2019t flesh and blood but \u201cprincipalities\u2026 powers\u2026 rulers of the darkness of this world\u2026 spiritual wickedness\u2026\u201d (Ephesians 6:12). Yet more powerful is the promise: \u201cResist the devil and he will flee from you\u201d (James 4:7).<\/p>\n\n\n\n
- Chunjiong Wang, Youfei Guan, and Jichun, \u201cCytokines in the Progression of Pancreatic \u03b2-Cell,\u201d International Journal of Endocrinology<\/em>, vol. 2010, Article ID 515136, 10 pages, 2010, https:\/\/www.hindawi.com\/journals\/ije\/2010\/515136\/.<\/li>
- Newcastle University, “Type 2 diabetes reversed by losing fat from pancreas,” ScienceDaily<\/em>, December 1, 2015, https:\/\/www.sciencedaily.com\/releases\/2015\/12\/151201141231.htm.<\/li><\/ol>\n","protected":false},"excerpt":{"rendered":"
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