No Pancreas, Gaining Weight, Wanting to Exercise

author : AMSSM
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Member Question

It is my understanding that Type 1 diabetics have no insulin (beta cell) production but probably have glucagon (alpha cell) production? I had my pancreas totally removed four months ago, I’m doing some exercise, struggling with the diabetes, and my usual slim frame is putting on weight and I don’t ever seem to feel full up after eating.
 
If you have time, your thoughts would be welcome. I’m in the UK and having your pancreas totally out seems so rare no-one seems to know the answers as to how different I am to a Type 1 diabetic.

Answer from Trent Christensen, MD
Member AMSSM

Given your recent history of pancreatectomy, you are suffering from a form of Diabetes Mellitus (DM) that falls under the category of “Diseases of the Exocrine Pancreas.” This category of diabetes is similar to the more common Type-1 DM in that neither has working Beta cells producing insulin, and both are forms of Insulin-Dependent Diabetes Mellitus (IDDM).  Unlike type-1 diabetics, however, you further suffer from a lack of all other pancreatic hormones and enzymes that are normally found in Type-1 DM, including glucagon (8). Interestingly, many Type-1 diabetics are less sensitive to the effects of glucagon; therefore, you are very comparable to many Type-1 diabetics (10).

Weight gain is common in people with Insulin Dependent Diabetes Mellitus (IDDM) and is likely multifactoral in nature. People on intensive insulin replacement programs gained an average of 4.8 kg over a six year period, with most of this weight gain seen within the first year of starting insulin therapy (2). In order to understand why IDDM patients gain weight, we must first have a basic understanding of insulin and glucagon.

Insulin is a hormone that is essential in regulating metabolism. Insulin has many roles, including: facilitating the uptake of sugar by cells, stimulating fat production while decreasing its breakdown, and increasing protein synthesis while decreasing its degradation.  The net effect is increased synthesis of carbs, fats, and proteins or, more simply, weight gain (9). Glucagon counteracts the actions of insulin, and as a result, causes a breakdown of carbs, fats, and proteins (10). Lack of glucagon is thus partially contributing to your weight gain. Additionally, insulin replacement therapy is less than optimal when compared to a person’s own physiological insulin secreting system and is another likely reason for weight gain. Insulin replacement therapy can intermittently elevate blood insulin levels to higher than normal physiologic levels, which as previously described, results in higher weight gain. Injected insulin is also more likely to distribute into the blood compared to the insulin released from your pancreas, which causes an increase in peripheral fat (7).  Also, people on insulin therapy often fear hypoglycemia, (low blood sugar) since the symptoms of hypoglycemia can be very unpleasant and even deadly.  Consequently, people are tempted to increase food consumption to decrease the likelihood of having hypoglycemic episodes (7).  

In addition, your temptation to overeat is hastened by your recent lack of satiety (a.k.a. feeling full). Satiety is the result of complex processes involving the interaction of the central nervous system with several different enzymes, hormones, and other factors secreted by the gastrointestinal system in response to food (11).  Some satiety signals are directly released from the pancreas (glucagon, somatostatin, amylin, enterostatin), whereas others are directly influenced by pancreatic secretions (CCK, GLP-1, Leptin, and Peptide YY) (1,4,11). A decrease or loss of these satiety signals could cause a person to remain hungry, even after eating. This could help explain your insatiable hunger and could further be contributing to your recent weight gain. Although the lack of satiety that you are now experiencing is likely partially secondary to the removal of your pancreas, it’s worth noting that personal and social habits, basic stressors, and/or other physiologic processes could be contributing (11).

Treatment of such problems can be complex and should be discussed with your doctor. Longer acting insulins have been shown to have less weight gain compared to shorter acting insulins and may be considered if you are not currently taking these (5). Other meds, including GLP-1 receptor agonists, have been used to increase satiety and facilitate weight loss in diabetics, and may be an option for you (4). A well-balanced diet with an emphasis on smaller portion size should be implemented. Studies have shown that increased meal size does not correlate with increased satiety. Thus, frequent small meals will likely decrease total daily caloric intake and be more satisfying (6).  Finally, a regular exercise program has been shown to reduce weight and may have an added benefit of decreasing the total daily insulin needed to treat diabetes (3,7).

Trent Christensen, MD
University of Minnesota 


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date: June 20, 2013

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The American Medical Society for Sports Medicine (AMSSM) was formed in 1991 to fill a void that has existed in sports medicine from its earliest beginnings. The founders most recognized and expert sports medicine specialists realized that while there are several physician organizations which support sports medicine, there has not been a forum specific for primary care non-surgical sports medicine physicians.

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The American Medical Society for Sports Medicine (AMSSM) was formed in 1991 to fill a void that has existed in sports medicine from its earliest beginnings. The founders most recognized and expert sports medicine specialists realized that while there are several physician organizations which support sports medicine, there has not been a forum specific for primary care non-surgical sports medicine physicians.

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