Objectives To evaluate the effect of pre-scan blood glucose levels (BGL) on standardized uptake value (SUV) in 18 F-FDG-PET scan. Methods A literature review was performed in the MEDLINE, Embase, and Cochrane library databases. Multivariate regression analysis was performed on individual datum to investigate the correlation of BGL with SUV max and SUV mean adjusting for sex, age, body mass index (BMI), diabetes mellitus diagnosis, 18 F-FDG injected dose, and time interval. The ANOVA test was done to evaluate differences in SUV max or SUV mean among five different BGL groups (< 110, 110-125, 125-150, 150-200, and > 200 mg/dl). Results Individual data for a total of 20,807 SUV max and SUV mean measurements from 29 studies with 8380 patients was included in the analysis. Increased BGL is significantly correlated with decreased SUV max and SUV mean in brain (p < 0.001, p < 0.001,) and muscle (p < 0.001, p < 0.001) and increased SUV max and SUV mean in liver (p = 0.001, p = 0004) and blood pool (p = 0.008, p < 0.001). No significant correlation was found between BGL and SUV max or SUV mean in tumors. In the ANOVA test, all hyperglycemic groups had significantly lower SUVs compared with the euglycemic group in brain and muscle, and significantly higher SUVs in liver and blood pool. However, in tumors only the hyperglycemic group with BGL of > 200 mg/dl had significantly lower SUV max. Conclusion If BGL is lower than 200 mg/dl no interventions are needed for lowering BGL, unless the liver is the organ of interest. Future studies are needed to evaluate sensitivity and specificity of FDG-PET scan in diagnosis of malignant lesions in hyperglycemia.

Impaired muscle strength and mass (sarcopenia) are common in patients with respiratory cachexia, namely chronic obstructive pulmonary disease (COPD) and in lung cancer (LC)‐cachexia. Misfolded/unfolded proteins in endoplasmic reticulum (ER) induce the compensatory unfolded protein response (UPR). Expression of ER stress and UPR markers may be differentially upregulated in vastus lateralis (VL) of patients with respiratory sarcopenia associated with either a chronic condition (COPD) or subacute (LC)‐cachexia. In VL specimens from 40 COPD patients (n = 21, sarcopenic, fat‐free mass index [FFMI] 16 kg/m2 and n = 19, nonsarcopenic, FFMI 18 kg/m2), 13 patients with LC‐cachexia (FFMI 17 kg/m2), and 19 healthy controls (FFMI 19 kg/m 2), expression markers of ER stress, UPR (protein kinase‐like ER kinase [PERK], activating transcription factor [ATF] 6, and inositol‐requiring enzyme [IRE] 1‐α), oxidative stress, autophagy, proteolysis, and apoptosis (reverse transcription polymerase chain reaction and immunoblotting), and fiber atrophy (histology) were assessed. Atrophy and muscle wasting and weakness were seen in both groups of sarcopenic patients. Compared to healthy controls, in muscles of LC‐cachexia patients, expression of ER stress markers and UPR (three arms) was significantly upregulated, while in sarcopenic COPD, expression of a few ER stress markers and IRE1‐α arm was upregulated. ER stress and an exaggerated UPR were observed in the VL muscle of patients with respiratory sarcopenia. The three branches of UPR were similarly upregulated in muscles of cancer cachectic patients, whereas in sarcopenic COPD patients, only IRE1 was upregulated. The differential profile of muscle UPR in chronic and subacute respiratory conditions offers a niche for the design of specific novel therapeutic approaches.

Sarcopenia is a major comorbidity in chronic obstructive pulmonary (COPD). Whether deficient muscle repair mechanisms and regeneration exist in the vastus lateralis (VL) of sarcopenic COPD remains debatable. In the VL of control subjects and severe COPD patients with/without sarcopenia, satellite cells (SCs) were identified (immunofluorescence, specific antibodies, anti‐Pax‐7, and anti‐Myf‐5): activated (Pax‐7+/Myf‐5+), quiescent/regenerative potential (Pax‐7+/Myf‐5‐), and total SCs, nuclear activation (terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling [TUNEL]), and muscle fiber type (morphometry and slow‐ and fast‐twitch, and hybrid fibers), muscle damage (hematoxylin‐eosin staining), muscle regeneration markers (Pax‐7, Myf‐5, myogenin, and MyoD), and myostatin levels were identified. Compared to controls, in VL of sarcopenic COPD patients, myostatin content, activated SCs, hybrid fiber proportions, TUNEL‐positive cells, internal nuclei, and muscle damage significantly increased, while quadriceps muscle strength, numbers of Pax‐7+/Myf‐5‐ and slow‐ and fast‐twitch, and hybrid myofiber areas decreased. In the VL of sarcopenic and nonsarcopenic patients, TUNEL‐positive cells were greater, whereas muscle regeneration marker expression was lower than in controls. In VL of severe COPD patients regardless of the sarcopenia level, the muscle regeneration process is triggered as identified by SC activation and increased internal nuclei. Nonetheless, a lower regenerative potential along with significant alterations in muscle phenotype and damage, and increased myostatin were prominently seen in sarcopenic COPD.