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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=
, 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
