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Bariatric Surgery in 2 weeks cures fatty liver and fatty pancreas

Rather than address the issue of fatty liver disease (NAFLD) as the underlying cause of T2D in the obese, the debate has been shifted on why there is for most patients a cure of T2D within the first 2 weeks following surgery (thus not because of weight loss) to GI hormone changes and surgery restricted food intake.  The restricted food intake causes a resolution of NALFD.   But the KOLs leave out NAFLD.  In other words, pharma has framed the topic of the cause of T2D in a way in which a dietary fix won’t work.  Very few obese patients will voluntarily undergo a fast comparable to that following bariatric surgery.    The article below while looking at the complex responses to bariatric surgery concludes that the reversal of fatty liver and fatty pancreas is central to the other changes.

A radical change in diet following surgery from extreme caloric restriction will produce a large number of changes in a regulatory system involving over 60 hormones.  However, I hold that it is not the hormonal changes that produces the cure for T2D, but rather the repair of the liver and pancreas via burning of excess fat in those tissues.  And below, this change has been shown to be essential, or at least resulting in a high cure rate.  (What is needed would be to test patients to see if some with NAFLD who are cured still have NAFLD.  The confound factor is that around 10% of those diagnose with T2D have been misdiagnosed and have adult onset T1D (LAD))

 

http://care.diabetesjournals.org/content/36/Supplement_2/S287.full 

1.       doi: 10.2337/dcS13-2032Diabetes Care August 2013vol. 36 no. Supplement 2 S287-S291

 

Mechanism of Metabolic Advantages After Bariatric Surgery

It’s all gastrointestinal factors versus it’s all food restriction

The predominant hypotheses on the physiological background for the metabolic advantages (specifically, the glucose-lowering effects) after bariatric surgery include changed release of GI hormones (increased secretion of hormones with antidiabetes properties and reduced secretion of “diabetogenic” hormones) and surgery-induced restriction of food intake. Here, the evidence for these two hypotheses will be scrutinized and compared to provide a robust analysis of current knowledge….

 

Its all GI track:  During recent years, it has become clear that the GI tract constitutes the largest and most varied endocrine organ of the body. More than 40 hormones originate from the GI tract, and several of these exert considerable impact on glucose metabolism and appetite regulation. The different GI hormones originate from specialized enteroendocrine cells scattered throughout the GI tract, with certain enteroendocrine cells located in specific regions and others more widespread and some with different density along the GI tract…. Whether bariatric surgery per se improves metabolic function via modifications of GI factors or purely via the low caloric intake in the first days after surgery remains controversial (8). However, data recently presented at the Annual Meeting of the European Association for the Study of Diabetes (21) showed that caloric restriction for a week (600 kcal/day resulting in 2.1 kg weight loss) or gastric banding had no effect on either hepatic or peripheral insulin sensitivity, whereas RYGB significantly improved both measures….

Confirmation that burning liver and pancreas fat cures T2D

[Acknowledgement of NAFLD}  The cataclysmic metabolic effect commencing on the day of surgery was that of sudden and profound negative calorie balance. The flow of carbon energy out of triglyceride stores must abruptly increase, and as ectopic fat stores are drawn on first in times of need, it could be predicted that liver fat levels would fall rapidly. This has previously been observed during modest calorie restriction (23). Liver fat level is closely related to hepatic insulin sensitivity for control of glucose production (23,24). It is therefore to be expected that fasting plasma glucose concentration would fall in step with liver fat. These predictions about pathophysiologic steps during the reversal of type 2 diabetes helped identify the time sequence of steps during the development of the condition, and this led directly to the twin cycle hypothesis of the etiology of type 2 diabetes (25). Hypotheses are testable. [#25. Taylor R.   Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause. Diabetologia 2008;51:1781–1789 CrossRefMedlineGoogle Schola]  For testing of the aspect of the twin cycle hypothesis relating to negative calorie balance, the Counterpoint study was conducted (26). The effects of a 600 kcal/day diet were examined in persons with up to 4 years’ duration of type 2 diabetes. In the first 7 days, mean fasting plasma glucose fell from 9.2 0.4 to 5.9 0.4 mmol/L. Simultaneously, liver fat levels fell 30% to the same level as those in nondiabetic control subjects and hepatic glucose production normalized (Fig. 2). An 8-week period of less severe calorie restriction has been shown to produce generally similar changes (23). The insulin sensitivity of the liver returned to normal in the 7-day period, but it is important to emphasize that muscle insulin sensitivity, reflected by the clamp technique, did not change at all. Acute, major negative calorie balance normalizes plasma glucose in type 2 diabetes.  Even more interestingly from the perspective of the etiology of type 2 diabetes, over the 8-week study period the pancreas fat level gradually fell to normal levels and both first-phase and total insulin response, measured by a gold standard method, gradually returned to normal (Fig. 3). Hence, the Counterpoint study established that two separate time courses in the reversal of type 2 diabetes could be identified: a rapid return of fasting metabolism to normal in step with a fall in liver fat and a slower return of β-cell function to normal in step with a fall in pancreatic fat.   During the 8 weeks of a very-low-calorie diet, mean body weight fell by 15.3 kg. No ongoing dietary input was provided after this intervention study, and mean body weight rose by 4 kg over the subsequent 12 weeks. At the end of this period, only 3 of 10 subjects retested had returned to a diabetic state based on oral glucose tolerance test criteria despite the weight gain (26). The study demonstrated that reversal of type 2 diabetes and restoration of normal β-cell function depend simply on reduction in intraorgan fat in liver and pancreas, and this can be produced by dietary means alone…. The major mechanism of the decrease in plasma glucose after bariatric surgery or hypocaloric dieting is not in doubt. Acute negative calorie balance is all that is needed to reverse type 2 diabetes.  [For those with BMI under 35 surgery had better results independent of years with T2D because their liver & pancreas fat mass is less than those with BMI above 35.]  It would appear that if intraorgan fat mass is not greatly elevated, there is a substantially greater chance of success of reducing it below the threshold level for diabetes for the individual. In these less obese subjects, there was no recurrence of diabetes over a median of 5 years of follow-up.

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http://care.diabetesjournals.org/content/36/Supplement_2/S287.full 

1.       doi: 10.2337/dcS13-2032Diabetes Care August 2013vol. 36 no. Supplement 2 S287-S291

 

Mechanism of Metabolic Advantages After Bariatric Surgery

It’s all gastrointestinal factors versus it’s all food restriction

The predominant hypotheses on the physiological background for the metabolic advantages (specifically, the glucose-lowering effects) after bariatric surgery include changed release of GI hormones (increased secretion of hormones with antidiabetes properties and reduced secretion of “diabetogenic” hormones) and surgery-induced restriction of food intake. Here, the evidence for these two hypotheses will be scrutinized and compared to provide a robust analysis of current knowledge….

 

Its all GI track:  During recent years, it has become clear that the GI tract constitutes the largest and most varied endocrine organ of the body. More than 40 hormones originate from the GI tract, and several of these exert considerable impact on glucose metabolism and appetite regulation. The different GI hormones originate from specialized enteroendocrine cells scattered throughout the GI tract, with certain enteroendocrine cells located in specific regions and others more widespread and some with different density along the GI tract…. Whether bariatric surgery per se improves metabolic function via modifications of GI factors or purely via the low caloric intake in the first days after surgery remains controversial (8). However, data recently presented at the Annual Meeting of the European Association for the Study of Diabetes (21) showed that caloric restriction for a week (600 kcal/day resulting in 2.1 kg weight loss) or gastric banding had no effect on either hepatic or peripheral insulin sensitivity, whereas RYGB significantly improved both measures….

Confirmation that burning liver and pancreas fat cures T2D

[Acknowledgement of NAFLD}  The cataclysmic metabolic effect commencing on the day of surgery was that of sudden and profound negative calorie balance. The flow of carbon energy out of triglyceride stores must abruptly increase, and as ectopic fat stores are drawn on first in times of need, it could be predicted that liver fat levels would fall rapidly. This has previously been observed during modest calorie restriction (23). Liver fat level is closely related to hepatic insulin sensitivity for control of glucose production (23,24). It is therefore to be expected that fasting plasma glucose concentration would fall in step with liver fat. These predictions about pathophysiologic steps during the reversal of type 2 diabetes helped identify the time sequence of steps during the development of the condition, and this led directly to the twin cycle hypothesis of the etiology of type 2 diabetes (25). Hypotheses are testable. [#25. Taylor R.   Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause. Diabetologia 2008;51:1781–1789 CrossRefMedlineGoogle Schola]  For testing of the aspect of the twin cycle hypothesis relating to negative calorie balance, the Counterpoint study was conducted (26). The effects of a 600 kcal/day diet were examined in persons with up to 4 years’ duration of type 2 diabetes. In the first 7 days, mean fasting plasma glucose fell from 9.2 0.4 to 5.9 0.4 mmol/L. Simultaneously, liver fat levels fell 30% to the same level as those in nondiabetic control subjects and hepatic glucose production normalized (Fig. 2). An 8-week period of less severe calorie restriction has been shown to produce generally similar changes (23). The insulin sensitivity of the liver returned to normal in the 7-day period, but it is important to emphasize that muscle insulin sensitivity, reflected by the clamp technique, did not change at all. Acute, major negative calorie balance normalizes plasma glucose in type 2 diabetes.  Even more interestingly from the perspective of the etiology of type 2 diabetes, over the 8-week study period the pancreas fat level gradually fell to normal levels and both first-phase and total insulin response, measured by a gold standard method, gradually returned to normal (Fig. 3). Hence, the Counterpoint study established that two separate time courses in the reversal of type 2 diabetes could be identified: a rapid return of fasting metabolism to normal in step with a fall in liver fat and a slower return of β-cell function to normal in step with a fall in pancreatic fat.   During the 8 weeks of a very-low-calorie diet, mean body weight fell by 15.3 kg. No ongoing dietary input was provided after this intervention study, and mean body weight rose by 4 kg over the subsequent 12 weeks. At the end of this period, only 3 of 10 subjects retested had returned to a diabetic state based on oral glucose tolerance test criteria despite the weight gain (26). The study demonstrated that reversal of type 2 diabetes and restoration of normal β-cell function depend simply on reduction in intraorgan fat in liver and pancreas, and this can be produced by dietary means alone…. The major mechanism of the decrease in plasma glucose after bariatric surgery or hypocaloric dieting is not in doubt. Acute negative calorie balance is all that is needed to reverse type 2 diabetes.  [For those with BMI under 35 surgery had better results independent of years with T2D because their liver & pancreas fat mass is less than those with BMI above 35.]  It would appear that if intraorgan fat mass is not greatly elevated, there is a substantially greater chance of success of reducing it below the threshold level for diabetes for the individual. In these less obese subjects, there was no recurrence of diabetes over a median of 5 years of follow-up.

 

 

^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^  Very good article with diagrams  -- need to read body of article

http://dst.sagepub.com/content/5/5/1263.full.pdf+html FULL   Journal of Diabetes Science and Technology

 Volume 5, Issue 5, September 2011

Mechanisms Responsible for Excess Weight Loss after Bariatric Surgery

Obesity has increased alarmingly in the United States and is increasing in many countries of the world. Because obesity is an important risk factor for type 2 diabetes and other chronic diseases, it is important to develop approaches to counter the rapid increase in adiposity. One approach is bariatric surgery, the most successful clinical intervention known for treating obesity. Surgery can result in impressive weight loss and improvement of obesity-related comorbidities. Yet the mechanisms responsible for this remarkable effect of surgery remain controversial. It is now clear that caloric restriction, per se, does not explain all the reduction in stored fat mass after surgery. A number of gastrointestinal hormones, including glucagon-like peptide (GLP)-1, peptide YY, oxyntomodulin, GLP-2, glucose-dependent insulinotropic polypeptide, ghrelin, and others, can play roles in energy homeostasis and could be involved in bariatric-surgery-related weight loss and weight loss maintenance. Vagal innervation may play a role. In addition, there may be other yet-uncharacterized factors that could participate. This review discusses the possible roles of these hormonal mechanisms in various types of bariatric surgery to help elucidate some of the potential mechanisms at play in short-term and long-term post-bariatric surgery weight loss. Understanding such mechanisms could lead to new and efficacious means to control or even reduce the epidemic of obesity.          

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An association of NAFLD with BMI > 40, and cure at 2 years out after surgery

http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1746.2007.04833.x/abstract?userIsAuthenticated=false&deniedAccessCustomisedMessage=

Volume 22, Issue 4, pages 510–514, April 2007

 

      Effects of bariatric surgery on nonalcoholic fatty liver disease: Preliminary findings after 2 years

 

Abstract

Background and Aim:  Although nonalcoholic fatty liver disease (NAFLD) is very common among morbidly obese patients, the effect of weight loss after bariatric surgery on inflammation and fibrosis related to NAFLD is still a matter of debate. The aim of this study was to evaluate the impact of Roux-en-Y gastric bypass (RYGB) surgery on NAFLD with a follow up of 2 years.

Methods:  Eighteen consecutive NAFLD patients with body mass index >40 kg/m2 undergoing gastroplasty with RYGB were enrolled, and wedge liver biopsy was obtained at the operation. After 2 years, these patients underwent percutaneous liver biopsy.

Results:  At baseline, 67% of patients had nonalcoholic steatohepatitis (NASH) and 33% had steatosis, according to the NASH Clinical Research Network Scoring System (NAS) for biopsy. Cirrhosis was present in 5.5% of the patients with NASH. After a mean excess weight loss of 60%, steatosis disappeared in 84% and fibrosis disappeared in 75% of the patients. Hepatocellular ballooning disappeared in 50%. A slight lobular inflammatory infiltrate remained in 81%, apparently unrelated to fatty degeneration. As liver biochemical variables had been found within normal limits in 92.3% of patients at initial biopsy, no difference was found 2 years later. Lipid profile and blood sugar plasma concentration were closer to normal in all patients after 2 years (P < 0.05).

Conclusions:  Aspects of NAFLD including steatohepatitis improved significantly with massive weight loss at 2 years after RYGB surgery. No patient in this series had progression of hepatic fibrosis.

  B

 


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