An interesting small study which fed subjects a very low fat diet and reversed their Type 2 Diabetes in a couple of months (Kitt Falk Petersen, Sylvie Dufour, Douglas Befroy, Michael Lehrke, Rosa E. Hendler, Gerald I. Shulman. Reversal of Nonalcoholic Hepatic Steatosis, Hepatic Insulin Resistance, and Hyperglycemia by Moderate Weight Reduction in Patients With Type 2 Diabetes. Diabetes Mar 2005, 54 (3) 603-608).
To examine the mechanism by which moderate weight reduction improves basal and insulin-stimulated rates of glucose metabolism in patients with type 2 diabetes, we used 1H magnetic resonance spectroscopy to assess intrahepatic lipid (IHL) and intramyocellular lipid (IMCL) content in conjunction with hyperinsulinemic-euglycemic clamps using [6,6-2H2]glucose to assess rates of glucose production and insulin-stimulated peripheral glucose uptake.
The participants were fed a low calorie, low fat diet.
Eight obese patients with type 2 diabetes were studied before and after weight stabilization on a moderately hypocaloric very-low-fat diet (3%).
These were full blown diabetic patients.
The diabetic patients were markedly insulin resistant in both liver and muscle compared with the lean control subjects. These changes were associated with marked increases in IHL (12.2 ± 3.4 vs. 0.6 ± 0.1%; P = 0.02) and IMCL (2.0 ± 0.3 vs. 1.2 ± 0.1%; P = 0.02) compared with the control subjects.
IHL is fat in the liver. The IHL went from 12.2% to 0.6% in the diabetics with the treatment.
A weight loss of only ∼8 kg resulted in normalization of fasting plasma glucose concentrations (8.8 ± 0.5 vs. 6.4 ± 0.3 mmol/l; P < 0.0005), rates of basal glucose production (193 ± 7 vs. 153 ± 10 mg/min; P < 0.0005), and the percentage suppression of hepatic glucose production during the clamp (29 ± 22 vs. 99 ± 3%; P = 0.003).
That is a fairly small weight loss but it shows that loss of fat from the liver drops the production of glucose from the liver significantly.
These improvements in basal and insulin-stimulated hepatic glucose metabolism were associated with an 81 ± 4% reduction in IHL (P = 0.0009)
These diabetics lost 81% of their liver fat!
but no significant change in insulin-stimulated peripheral glucose uptake or IMCL (2.0 ± 0.3 vs. 1.9 ± 0.3%; P = 0.21).
This showed it wasn’t peripheral Insulin Resistance that was the problem, but rather fat in the liver. It also wasn’t other fat (IMCL).
In conclusion, these data support the hypothesis that moderate weight loss normalizes fasting hyperglycemia in patients with poorly controlled type 2 diabetes by mobilizing a relatively small pool of IHL, which reverses hepatic insulin resistance and normalizes rates of basal glucose production, independent of any changes in insulin-stimulated peripheral glucose metabolism.
The average course of treatment was 7 weeks. After the treatment their Fasting Insulin levels were almost 1/3 of the original numbers.
Low carb, of course, can quickly achieve the same results but this does point to the liver fat as the root cause of diabetes. I did this in two weeks with Low Carb and Intermittent Fasting.
Bariatric patients who are scheduled surgery are often told that they need to lose liver fat before their surgery. From (How to Shrink Your Liver Before Weight Loss Surgery).:
Studies have shown that losing weight before surgery and avoiding carbohydrates and fats in the weeks leading up to surgery can reduce the size of your liver through a process known as “ketosis,” which is when your body starts to use its fat stores because it has run out of fuel (calories). Excess fat in the liver appears to be one of the first places the body turns to for this added fuel.
Or you can just stay on the Low Carb diet…
A Second Related Study
Here’s a second related study (Noud A. van Herpen Vera B. Schrauwen-Hinderling Gert Schaart Ronald P. Mensink Patrick Schrauwen. Three Weeks on a High-Fat Diet Increases Intrahepatic Lipid Accumulation and Decreases Metabolic Flexibility in Healthy Overweight Men. The Journal of Clinical Endocrinology & Metabolism, Volume 96, Issue 4, 1 April 2011, Pages E691–E695).
Twenty overweight men were randomly allocated to low- or high-fat groups (age, 54.0 ± 2.3 and 56.4 ± 2.5 yr; body mass index, 29.3 ± 0.6 and 28.3 ± 0.5 kg/m2, respectively). Both groups started with a 3-wk low-fat diet [15% energy (En%) as protein, 65 En% as carbohydrates, 20 En% as fat], after which half of the subjects switched to a 3-wk isocaloric high-fat diet (15 En% protein, 30 En% carbohydrates, 55 En% fat). After 3 and 6 wk, IHL and IMCL content were assessed by 1H magnetic resonance spectroscopy and a muscle biopsy, and insulin sensitivity was studied using a hyperinsulinemic-euglycemic clamp. An additional liver scan was performed after 1 wk in the high-fat group.
Note this was not a low carb study because both diets were relatively high in carbohydrates. However, the results are interesting.
IHL decreased by 13% in the low-fat group and increased by 17% in high-fat group (P = 0.047). IMCL content was unaffected (P = 0.304). Insulin sensitivity was unaffected. At wk 3, IHL correlated negatively with insulin sensitivity (r = −0.584; P = 0.009, all subjects combined). Metabolic flexibility, defined as change in respiratory quotient upon insulin stimulation, was decreased after 3 wk of the high-fat diet (change in respiratory quotient was +0.02 ± 0.02 vs.−0.05 ± 0.1 in low-fat vs. high-fat group, P = 0.009).
The change in RQ was very small which shows that the carb/fat burning mixture was not much changed. There was enough carbs present to cause the liver to get fatter.