Episode 38 - Fatty pancreas, fatty liver and diabetes
Raphael asks Gabor what’s wrong with a fatty pancreas? Why do we care whether or not our pancreas is fatty?
Gabor says pancreatic was thought to be particularly bad compared to other ectopic fat (e.g. intra-abdominal fat), which is one reason why so much attention is paid to it.
Raphael mentions that there are studies finding no issues in insulin secretion capacity in people with a fatty pancreas.
Gabor explains that diabetics have ‘lower than necessary’ insulin secretion – not just merely ‘lower than normal’. Their insulin is ‘relatively low’ meaning it’s insufficient to make up for their general extent of insulin resistance.
Raphael goes over Roy Taylor’s 2016 study lasting +6-month where type 2 diabetics were put on a very low-calorie diet (initially).
Gabor talks about the ‘shake’ used in the very low-calorie part of the study called Optifast.
Raphael asks Gabor if he agrees with Roy Taylor’s ‘not diabetic’ cut-off of < 7 mmol/L. Long story short, Gabor disagrees.
Raphael mentions that the people in Roy Taylor’s study, eating about one third of their maintenance calories over 2 months, went from 99.8 kg to 84.1 kg (-15.7 kg) in the Responders group and 96.7 kg to 83.6 kg (-13.1 kg) in the Non-Responder’s.
Gabor asks Raphael what he’d rather eat during those 2 months at ~ 700 kilocalories per day? Raphael says eggs and liver!
Raphael explains what the Responders and Non-Responders are in Roy Taylor’s study – and why it’s a bit of a misnomer.
Raphael explains why it’s said some people have ‘relative insulin deficiency’ and that it’s based on fasting ketone levels (which are higher when relatively deficient in insulin). Gabor then connects it all to high FFAs (free fatty acid).
Gabor highlights that the average decrease in the pancreatic fat of Non-responders was equally extensive (and more statistically significant) compared to so-called Responders! Hence, the misnomer of Responders vs Non-Responders.
Raphael asks Gabor to explain what the Fat Threshold is and why it might help us understand obesity and ectopic fat deposition.
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Raphael explains that, instead of Optifast, a diet of much higher quality could be devised to sustainably lower the total amount of fat spilling over the personal fat thresholds as well as normalize appetite and generally improve metabolic function.
Raphael asks Gabor thinks about the instances where a fatty pancreas doesn’t seem to fail to appropriately secrete insulin.
Gabor explains that the liver seems more sensitive to ectopic fat deposition than the pancreas.
Gabor summarizes the results from the 2017 Japanese autopsy study, showing that pancreatic fat was not a good predictor of pancreatic function or of type 2 diabetes
“While IPFA was positively correlated with age and BMI, there was no significant difference in IPFA between cases with and without diabetes. Moreover, no association was found between IPFA and either beta or alpha cell area, or HbA1c. Conclusion: These findings suggest that pancreatic fat deposits have little effect on beta cell mass and the development of diabetes in humans”
Raphael quotes from a study called “Dysregulated lipid storage and its relationship with insulin resistance and cardiovascular risk factors in non-obese Asian patients with type 2 diabetes” by Rattarasarn (2018)
“These cells respond to surplus energy through processes of proliferation or expansion so called adipocyte hyperplasia or adipocyte hypertrophy, respectively”
Raphael suggests the causality could maybe also be reversed, whereby adipocyte hypertrophy and/or hyperplasia happens first, leading to behavior changes that ‘fill the adipocyte’ (going into a positive energy balance)
Gabor raises an interesting question for future podcasts ‘What causes subcutaneous fat dysfunction?’