Does "Fatty Pancreas" Cause Type 2 Diabetes?

[Dean Pomerleau]

There has been some concern over the years among CR practitioners about the possibility of diabetes, largely based on observations that some of us don't do very well on an oral glucose tolerance test (OGTT). But by-and-large we are highly sensitive to insulin (unlike type 2 diabetics and pre-diabetics).

 

Some of us suspect our poor OGTT response may simply be a result of our pancreas being 'out of practice' - not having to pump out that much insulin on a regular basis, because of our low glycemic index / glycemic load diet, and because we eat fewer calories than most people. But others have a lingering worry that for whatever reason (perhaps related to the idea of 'use it or lose it'?), insulin producing beta-cells in our pancreas may be dying or atrophying, potentially making us susceptible to diabetes somewhere down the line...

 

Anyway, with that background, I found this new study [1], discussed in Science Daily, to be both very interesting and potentially comforting for us skinny folk. It found that weight loss following gastric bypass surgery resulted not just in normal (visceral and subcutaneous) fat loss. It found that loss of fat accumulations in the pancreas also occurred, but only in the type II diabetics they were studying, not in the obese, but otherwise metabolically healthy, controls.  

 

The authors claim it was the loss of pancreatic fat that caused the reversal of the glucose intolerance in the diabetics via a reversal of their attenuated first-phase insulin response.

 

At least in the Science Daily coverage, the authors are suggesting that fat 'clogging' the pancreas may in fact be the underlying cause of Type 2 diabetes:

 

Previous work by Professor Taylor and his team highlighted the importance of weight loss through diet in reversing Type 2 diabetes. This work in 2011 transformed the thinking in diabetes as it was the first time that it had been demonstrated that diet could remove fat clogging up the pancreas allowing normal insulin secretion to be restored.

 

Professor Taylor adds: "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."

 

Since it would seem unlikely that we CR folks would be accumulating fat in our pancreas (since we don't accumulate it anywhere else), we should be safe from this apparent cause of Type 2 diabetes at least.

 

--Dean

 

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[1] Diabetes Care, December 2015 DOI: 10.2337/dc15-0750

 

 Sarah Steven, Kieren G. Hollingsworth, Peter K. Small, Sean A. Woodcock, Andrea Pucci, Benjamin Aribisala, Ahmad Al-Mrabeh, Ann K. Daly, Rachel L. Batterham, and Roy Taylor. 

 

Weight Loss Decreases Excess Pancreatic Triacylglycerol Specifically in Type 2 Diabetes.

 

 

Abstract

 

OBJECTIVE This study determined whether the decrease in pancreatic triacylglycerol during weight loss in type 2 diabetes mellitus (T2DM) is simply reflective of whole-body fat or specific to diabetes and associated with the simultaneous recovery of insulin secretory function.

 

RESEARCH DESIGN AND METHODS Individuals listed for gastric bypass surgery who had T2DM or normal glucose tolerance (NGT) matched for age, weight, and sex were studied before and 8 weeks after surgery. Pancreas and liver triacylglycerol were quantified using in-phase, out-of-phase MRI. Also measured were the first-phase insulin response to a stepped intravenous glucose infusion, hepatic insulin sensitivity, and glycemic and incretin responses to a semisolid test meal.

 

RESULTS Weight loss after surgery was similar (NGT: 12.8 ± 0.8% and T2DM: 13.6 ± 0.7%) as was the change in fat mass (56.7 ± 3.3 to 45.4 ± 2.3 vs. 56.6 ± 2.4 to 43.0 ± 2.4 kg). Pancreatic triacylglycerol did not change in NGT (5.1 ± 0.2 to 5.5 ± 0.4%) but decreased in the group with T2DM (6.6 ± 0.5 to 5.4 ± 0.4%; P = 0.007). First-phase insulin response to a stepped intravenous glucose infusion did not change in NGT (0.24 [0.13–0.46] to 0.23 [0.19–0.37] nmol ⋅ min−1 ⋅ m−2) but normalized in T2DM (0.08 [−0.01 to –0.10] to 0.22 [0.07–0.30]) nmol ⋅ min−1 ⋅ m−2 at week 8 (P = 0.005). No differential effect of incretin secretion was observed after gastric bypass, with more rapid glucose absorption bringing about equivalently enhanced glucagon-like peptide 1 secretion in the two groups.

 

CONCLUSIONS The fall in intrapancreatic triacylglycerol in T2DM, which occurs during weight loss, is associated with the condition itself rather than decreased total body fat.