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Maternal serum alpha-fetoprotein (MSAFP) values are reported to be lower in type 1 diabetic patients, and a correction factor is often applied.
In addition, intrapatient variability is likely to be lower in type 1 diabetes because of the lack of substantial endogenous insulin production.
Again, acetate recovery tended to be lower in type 2 diabetic patients and IGT individuals compared with healthy controls (about 63, 63 and 71%, in type 2 diabetes mellitus, IGT and controls, respectively, n = 7, p = 0.07).
Subsarcolemmal mitochondria content has been found to be lower in type 2 diabetes, although this could possibly be due to decreased levels of physical activity of the subjects (38).
Remarkably, even after correction for factors related to mitochondrial function, which actually may differ between diabetic patients and control individuals, like RQ, obesity (as defined by body fat%) and metabolic rate (workload), the ARF tended to be lower in type 2 diabetic patients compared with obese and lean controls [ 8].
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Although EHD2 was enriched in isolated LB, the signal was lower in type II cells compared to whole lung lysate, suggesting that EHD2 may be expressed in multiple lung cell types (Figure 5C).
Indeed, the expression of complement receptor 3 on monocytes from non-insulin-dependent diabetes patients was strongly decreased and the CD55 and CD59 complement regulatory protein-positive monocytes were lower in type 2 diabetic patients [33] [36].
Total adipocyte cellularity is lower in type 2 diabetic subjects than in obese subjects.
Amino acid concentrations were lower in type 2 diabetes compared with NW.
As expected, GSIS and the adipose disposition index were lower in type 2 diabetic compared with nondiabetic subjects (P < 0.05; Table 1).
Our results revealed that plasma Gas6 values were lower in type 2 diabetes and also negatively correlated with inflammation markers including TNF-α and IL-6.
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