No Pancreas, Gaining Weight, Wanting to Exercise

author : AMSSM

comments : 0

I had my pancreas 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

Member Question

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 

1. Balagopal PB, Gidding SS, Buckloh LM, et al. Changes in circulating satiety hormones in obese children: A randomized controlled physical Activity-Based intervention study. Obesity. 2010;18(9):1747-1753.

2. Care D. Influence of intensive diabetes treatment on body weight and composition of adults with type 1 diabetes in the diabetes control and complications trial. Diabetes Care. 2001;24(10):1711-1721.

3. Carver C. Insulin treatment and the problem of weight gain in type 2 diabetes. Diabetes Educ. 2006;32(6):910-917.

4. D'Alessio D. Intestinal hormones and regulation of satiety: The case for CCK, GLP-1, PYY, and apo A-IV. J Parenter Enteral Nutr. 2008;32(5):567-568.

5. De Leeuw I, Vague P, Selam J, et al. Insulin detemir used in basal-bolus therapy in people with type 1 diabetes is associated with a lower risk of nocturnal hypoglycaemia and less weight gain over 12 months in comparison to NPH insulin. Diabetes, Obesity and Metabolism. 2005;7(1):73-82.

6. Ello-Martin JA, Ledikwe JH, Rolls BJ. The influence of food portion size and energy density on energy intake: Implications for weight management. Am J Clin Nutr. 2005;82(1):236S-241S.

7. Khan R. Weight gain and insulin therapy. The British Journal of Diabetes & Vascular Disease. 2004;4(4):264-267.

8. MELLITUS D. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2011;27:S5-S10.

9. Newsholme E, Dimitriadis G. Integration of biochemical and physiologic effects of insulin on glucose metabolism. Experimental and Clinical Endocrinology & Diabetes. 2001;109(Suppl 2):S122-S134.

10. Siafarikas A, Johnston RJ, Bulsara MK, O’Leary P, Jones TW, Davis EA. Early loss of the glucagon response to hypoglycemia in adolescents with type 1 diabetes. Diabetes Care. 2012;35(8):1757-1762.

11. Woods SC. Gastrointestinal satiety signals I. an overview of gastrointestinal signals that influence food intake. American Journal of Physiology-Gastrointestinal and Liver Physiology. 2004;286(1):G7-G13. 

Rating

Click on star to vote

13363 Total Views  |  17 Views last 30 days  |  6 Views last 7 days

date: June 20, 2013