Brown adipose tissue detected by PET/CT imaging is associated with less central obesity.

PURPOSE: This retrospective review was performed to determine whether patients with brown adipose tissue (BAT) detected by fluorine-18-fluorodeoxyglucose (F-FDG) PET/computed tomography (CT) imaging have less central obesity than BMI-matched control patients without detectable BAT. PATIENTS AND METHODS: Thirty-seven adult oncology patients with F-FDG BAT uptake were retrospectively identified from PET/CT studies from 2011 to 2013. The control cohort consisted of 74 adult oncology patients without detectable F-FDG BAT uptake matched for BMI/sex/season. Tissue fat content was estimated by CT density (Hounsfield units) with a subsequent noise removal step. Total fat and abdominal fat were calculated. An automated separation algorithm was utilized to determine the visceral fat and subcutaneous fat at the L4/L5 level. In addition, liver density was obtained from CT images. CT imaging was interpreted blinded to clinical information. RESULTS: There was no difference in total fat for the BAT cohort (34±15 l) compared with the controls (34±16 l) (P=0.96). The BAT cohort had lower abdominal fat to total fat ratio compared with the controls (0.28±0.05 vs. 0.31±0.08, respectively; P=0.01). The BAT cohort had a lower visceral fat/(visceral fat+subcutaneous fat) ratio compared with the controls (0.30±0.10 vs. 0.34±0.12, respectively; P=0.03). Patients with BAT had higher liver density, suggesting less liver fat, compared with the controls (51.3±7.5 vs. 47.1±7.0 HU, P=0.003). CONCLUSION: The findings suggest that active BAT detected by F-FDG PET/CT is associated with less central obesity and liver fat. The presence of foci of BAT may be protective against features of the metabolic syndrome.

Estimation of glucose utilization in a type 2 diabetes mellitus patient on insulin analogs with tumor hypoglycemia induced by IGF-II.

We present a 38-year-old male patient with insulin requiring type 2 diabetes mellitus (DM) who had fasting hypoglycemia caused by a non-pancreatic-islet-cell mesenchymal tumor producing IGF-II. The evaluation was confounded in that there was pre-existing DM being treated with insulin analogs. Insulin levels were assessed with an immunoassay with cross reactivity with the insulin analogs. An 18-Fluorodeoxyglucose (FDG) positron emission tomography/computerized tomography (PET/CT) scan localized the 19.7×18.0×17.8cm retroperitoneal mass. A 3.25kg tumor was resected. Post-operatively insulin treatment was resumed and circulating IGF-II levels returned to normal. The maximum standardized uptake values of FDG (SUVmax) along with a steady state glucose infusion of 17.5g/h were used to determine the components of glucose utilization due to IGF-II induced muscle glucose uptake (utilization, 62%) whereas the tumor itself was responsible for approximately 22% of measurable glucose uptake. Whereas tumor induced hypoglycemia has been ascribed to preferential glucose utilization by the tumor, the predominant hypoglycemic effect was due to hormonal IGF-II induced total body glucose uptake.

Evidence for structural symmetry and functional asymmetry in the lactose permease of Escherichia coli.

Previous work on the lactose permease of Escherichia coli has shown that mutations along a face of predicted transmembrane segment 8 (TMS-8) play a critical role in conformational changes associated with lactose transport (Green, A. L., and Brooker, R. J. [2001] Biochemistry 40, 12220-12229). Substitutions at positions 261, 265, 268, 272, and 276, which form a continuous stripe along TMS-8, were markedly defective for lactose transport velocity. In the current study, three single mutants (F261D, N272Y, N272L) and a double mutant (T265Y/M276Y) were chosen as parental strains for the isolation of mutants that restored transport function. A total of 68 independent mutants were isolated and sequenced. Forty-four were first-site revertants in which the original mutation was changed back to the wild-type residue or to a residue with a similar side-chain volume. The other 24 mutations were second-site suppressors in TMS-2 (Q60L, Q60P), loop 2/3 (L70H), TMS-7 (V229G/A), TMS-8 (F261L), and TMS-11 (F354V, C355G). On the basis of their locations, the majority of the second-site suppressors can be interpreted as improving the putative TMS-2/TMS-7/TMS-11 interface to compensate for conformational defects imposed by mutations in TMS-8 that disrupt the putative TMS-1/TMS-5/TMS-8 interface. Overall, this paper suggests that the TMS-2/TMS-7/TMS-11 interface is more important from a functional point of view, even though there is compelling evidence for structural symmetry between the two halves of the permease.