2 research outputs found
Bile Acid Malabsorption in Cystic Fibrosis; Membrane Vesicles, a Tool for Revealing the Role of the Ileal Brush Border Membrane
ABSTRACT. Increased fecal bile acid loss in cystic fibrosis (CF) may result from ileal dysfunction. A method to quantitate in vitro Na+‐dependent taurocholate uptake into brush border membrane vesicles prepared from frozen ileum and ileal biopsy specimen is described. This transport across the ileal brush border membrane can be measured selectively, in contrast to in vivo measurements which represent a complex overall process. Preliminary results obtained with ileal specimen of 2 CF patients, suggest that in vitro bile acid uptake is low but not abnormal. Copyrigh
Weight loss and elevated gluconeogenesis from alanine in lung cancer patients
BACKGROUND: The role of gluconeogenesis from protein in the pathogenesis
of weight loss in lung cancer is unclear. OBJECTIVE: Our aim was to study
gluconeogenesis from alanine in lung cancer patients and to analyze its
relation to the degree of weight loss. DESIGN: In this cross-sectional
study, we used primed-constant infusions of [6,6-(2)H(2)]-D-glucose and
[3-(13)C]-L-alanine to assess whole-body glucose and alanine turnover and
gluconeogenesis from alanine in weight-losing (WL, n = 9) and
weight-stable (WS, n = 10) lung cancer patients and healthy control (n =
15) subjects. RESULTS: Energy intake and plasma alanine concentrations did
not differ significantly among the subject groups. Mean (+/-SEM)
whole-body glucose production was significantly higher in WL than in WS
and control subjects (0.74 +/- 0.06 compared with 0.55 +/- 0.04 and 0.51
+/- 0.04 mmol*kg(-)(1)*h(-)(1), respectively, P < 0.01). Alanine turnover
was significantly elevated in WL compared with WS and control subjects
(0.57 +/- 0.04 compared with 0.42 +/- 0.05 and 0.40 +/- 0.03
mmol*kg(-)(1)*h(-)(1), respectively, P < 0.01). Gluconeogenesis from
alanine was significantly higher in WL than in WS and control subjects
(0.47 +/- 0.04 compared with 0.31 +/- 0.04 and 0.29 +/- 0.04
mmol*kg(-)(1)*h(-)(1), respectively, P < 0.01). The degree of weight loss
was positively correlated with glucose and alanine turnover and with
gluconeogenesis from alanine (r = 0.45 for all, P < 0.01). CONCLUSIONS:
Aberrant glucose and alanine metabolism occurred in WL lung cancer
patients. These changes were related to the degree of weight loss and not
to the presence of lung cancer per se