Insulin Signaling in Human Visceral and Subcutaneous Adipose Tissue In Vivo
This is what they found. The black squares are the omental fat:
The x axis is non linear. Insulin signaling kicks in much faster in visceral adipocytes and is more effective at activating the whole signaling cascade (phosphorylation of AKT included) than it is in subcutaneous adipocytes. As the authors comment:
"We show that visceral fat is characterized by higher expression levels of specific insulin signaling proteins and more pronounced and earlier activation of the insulin receptor, Akt, glycogen synthase kinase (GSK)-3, and ERK-1/2 in response to insulin".
EDIT: Just look at those basal relative IR phosphorylation levels, visceral adipocytes have four times the insulin signaling as subcutaneous adipocytes after an overnight pre-surgical fast. I love this paper. END EDIT.
I think that it is unarguable that visceral adipocytes are more insulin sensitive than subcutaneous adipocytes.
Just to confirm that bias, this next paper is looking at glucose uptake in volunteers, using all sorts of clever non-invasive techniques. And some of those volunteers were obese. I think it's very clear that visceral fat, under hyperinsulinaemic euglycaemic clamp conditions, is more insulin sensitive than subcutaneous fat. Any visceral fat, any subcutaneous fat, any bodyweight of owner. From this paper
Glucose uptake and perfusion in subcutaneous and visceral adipose tissue during insulin stimulation in nonobese and obese humans
we have this:
First and 4th pairs of columns are SC adipose tissue, 2nd and 3rd are visceral. Even in obese subjects the glucose uptake by visceral fat, under clamp conditions, is higher than in SC adipose tissue. Lots of significant p values.
Now the flip side, rather more speculative here: let's revisit this paper from several years ago, looking at healthy humans under hypoinsulinaemic states:
Prolonged Fasting Identifies Skeletal Muscle Mitochondrial Dysfunction as Consequence Rather Than Cause of Human Insulin Resistance
Ignore the mindset of the researchers, just look at their data:
In a normally fed Dutchman the fasting FFAs are around 0.2mmol/l at some time in the morning. This is the amount of FFAs being released under a plasma insulin of about 13.0microU/ml. At this level of insulin I very much doubt if any of these FFAs are coming from visceral adipocytes because insulin is still too high for this. This a workaday "ready for breakfast" sort of a combination of FFAs and insulin. I think it is very reasonable to consider that these FFAs are coming primarily from the subcutaneous adipose stores.
By 36 hours of fasting insulin has dropped to around 7.0microU/ml and it stays there. At this level of insulin we have FFAs rising through 1.0mmol/l to 2.0mmol/l, that's very high. Insulin is now very low, low enough for visceral fat to release a lot of FFAs and the body is set up to run on fat and ketones. It could do with some hepatic insulin resistance to facilitate hepatic glucose output and the specifically portal vein draining fat depots (omental and mesenteric) are set up to do exactly this. Evolution has punished, by non survival, individuals who failed to follow this pattern.
I think it is a pretty sound case that visceral fat does very little, other than hoover up a few calories, while ever insulin is above 12microU/ml. In the USA insulin probably never falls below this level. If you have to get up at 2am for a few bagels, doughnuts or a bucket of (low fat/high sugar) ice cream your body will forget what an insulin of 12microU/ml ever felt like.
Visceral fat is a surrogate for chronic hyperinsulinaemia. It will be associated with metabolic syndrome because hyperinsulinaemia, not visceral fat, is metabolic syndrome. Given that nice, clear cut, pretty water tight case, what should a bariatric surgeon do about omental fat?
Why not chop it out? I mean its full of fat. All people who have metabolic syndrome have tons of the stuff. Really, it has to be the root of all evil. You know, fat... But:
Hepatic and Peripheral Insulin Sensitivity and Diabetes Remission at 1 Month After Roux-en-Y Gastric Bypass Surgery in Patients Randomized to Omentectomy
"Peripheral insulin sensitivity did not improve 1 month after RYGB, irrespective of omentectomy, diabetes, or diabetes remission. Hepatic insulin sensitivity improved at 1 month after RYGB and was more pronounced in patients with diabetes..." [but not associated with omentectomy, my addition]
Potential Additional Effect of Omentectomy on Metabolic Syndrome, Acute-Phase Reactants, and Inflammatory Mediators in Grade III Obese Patients Undergoing Laparoscopic Roux-en-Y Gastric Bypass
"Omentectomy does not have an ancillary short-term significant impact on the components of metabolic syndrome and does not induce important changes in the inflammatory mediators in patients undergoing LRYGB. Operative time is more prolonged when omentectomy is performed".
A prospective randomized study comparing patients with morbid obesity submitted to sleeve gastrectomy with or without omentectomy
"The theoretical advantages of omentectomy in regard to weight loss and obesity-related abnormalities are not confirmed in this prospective study. Furthermore, omentectomy does not induce important changes in the inflammatory status in patients undergoing SG".
These people got paydirt:
Omentectomy added to Roux-en-Y gastric bypass surgery: A randomized, controlled trial
"Omentectomy added to a LRYGB results in favorable changes in glucose homeostasis, lipid levels, and adipokine profile at 90-days"
but the changes were small and didn't look particularly clinically significant to me. But then, I am very biased. Better hope this last group aren't effective medical politicos!
Bottom line: Visceral fat does not cause metabolic syndrome. Association is not causation. Omentectomy is no panacea (no sniggering at the back there) unless you come from Oregon, with apologies to more sensible folks from Oregon.