Pancreatic cancer affects the body’s ability to regulate blood sugar. The tumor’s presence often leads to the development of high blood sugar (hyperglycemia) or significantly worsens pre-existing diabetes. This disruption can manifest as new-onset diabetes, which may appear months before a cancer diagnosis, offering an important diagnostic signal. Understanding this connection requires examining the pancreas’s unique functions and the biological assault the cancer launches on the metabolic system.
The Pancreas’s Dual Role in Blood Sugar Regulation
The pancreas, an elongated organ situated behind the stomach, performs two distinct roles. Its larger function is its exocrine role, involving the production of digestive enzymes like amylase and lipase, which flow into the small intestine to break down food.
The other function is its endocrine role, responsible for maintaining the body’s energy balance. Within the pancreatic tissue are clusters of cells called the Islets of Langerhans, which secrete hormones directly into the bloodstream.
The two main hormones produced are insulin and glucagon, which work in opposition to keep blood glucose levels stable. Insulin, secreted by beta cells, lowers blood sugar by signaling cells to absorb glucose. Conversely, glucagon is released by alpha cells to signal the liver to release stored glucose. Pancreatic cancer directly compromises this system, interfering with both insulin production and effectiveness.
Direct Mechanisms Causing High Blood Sugar
Pancreatic tumors cause high blood sugar through two primary mechanisms: physical destruction of insulin-producing cells and systemic insulin resistance. The tumor mass physically damages the Islets of Langerhans, diminishing the total number of beta cells available to produce insulin. This results in a direct loss of the body’s capacity to lower blood glucose, similar to Type 1 diabetes.
The more complex mechanism involves the tumor releasing substances that cause insulin resistance throughout the body. Cancer cells and surrounding inflamed tissue secrete various molecules, such as micro-RNAs and specific cytokines. These factors interfere with the communication pathways that allow insulin to work effectively in distant tissues.
This interference means that even if the pancreas produces insulin, the body’s cells do not respond correctly to the hormone’s signal. The glucose remains in the bloodstream, leading to hyperglycemia. This resistance is often a “post-receptor defect,” meaning the problem lies in the internal cellular machinery responsible for absorbing glucose.
This systemic insulin resistance forces the remaining healthy beta cells to overproduce insulin in a compensatory effort. Over time, these overworked cells may fail, further contributing to the severity of the diabetes. The tumor impairs the body’s ability to use insulin while reducing the pancreas’s capacity to produce it.
New-Onset Diabetes as a Potential Diagnostic Signal
The development of new-onset diabetes (NOD) can be an early warning sign of pancreatic cancer. Studies show that up to 25% of pancreatic cancer patients are diagnosed with diabetes six to 36 months before their cancer is discovered. This suggests the tumor causes metabolic changes before noticeable physical symptoms appear.
The risk of pancreatic cancer is nearly eightfold higher in older individuals who develop NOD compared to the general population. This cancer-associated diabetes often lacks the typical risk factors of Type 2 diabetes, such as long-term obesity or a strong family history.
Patients with NOD linked to pancreatic cancer frequently experience rapid and unexplained weight loss, a feature less common in standard Type 2 diabetes. This phenomenon creates a “window of opportunity” for earlier detection in high-risk groups.
Clinicians are working to differentiate pancreatic cancer-associated diabetes from the more common forms. Diagnostic tools, such as the Enriching New-onset Diabetes for Pancreatic Cancer (ENDPAC) score, use factors like age, recent weight loss, and the rise in blood glucose levels to identify those who should be screened for underlying cancer.
Managing Blood Sugar Alongside Pancreatic Cancer
Managing blood sugar in a patient with pancreatic cancer presents unique challenges, often classifying the condition as Type 3c diabetes. The fluctuating nature of the tumor’s activity and side effects from treatments like chemotherapy can lead to unpredictable swings in blood glucose, requiring frequent adjustments to medication.
A particular danger is the risk of hypoglycemia (dangerously low blood sugar) due to poor appetite, weight loss, and the catabolic effects of the cancer. Patients often rely on injected insulin, as many oral diabetes medications are less effective in this setting. The goal is to maintain glucose control while minimizing the risk of severe low-sugar events.
A complication arises with Pancreatic Enzyme Replacement Therapy (PERT), which is necessary to help patients digest food. By improving carbohydrate absorption, PERT can cause blood sugar levels to rise, requiring an increase in diabetes medication. This necessitates close collaboration between the oncology team, a diabetes specialist, and a dietitian.
If the tumor is successfully removed through surgery, the diabetes caused by the cancer often improves or can even resolve completely. Close monitoring remains necessary after surgery to manage the body’s recovery and metabolic recalibration.