Osteoporosis and Hepatic Steatosis: 2 Closely Related Complications in Short-Bowel Syndrome.

BACKGROUND: Osteoporosis has scarcely been prospectively investigated in short-bowel syndrome (SBS). This prospective study was designed to evaluate incretins, adipokines, bone mass, and lipid deposits from marrow adipose tissue (MAT), visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and liver (IHLs). METHODS: The study comprised 2 groups matched by gender, height, and age: the control group (CG) (9 males, 9 females) and the SBS group (SBSG) (6 males, 5 females). The SBSG was evaluated twice in an interval of 1 year (SBSG0 and SBSG1 ). The biochemical evaluation included incretins, leptin, and adiponectin. Dual-energy x-ray absorptiometry and magnetic resonance were, respectively, used to measure BMD and lipid deposits. RESULTS: Bone mineral density (BMD) was lower in the SBSG than in the CG, but there was no difference between SBSG0 and SBSG1 . There was no difference in MAT, SAT, and VAT, but IHL was lower in CG than in SBSG0 and SBSG1 . A negative correlation between MAT and third lumbar vertebrae BMD was found in the CG but not in SBSG0 or SBSG1 . There was a negative association between IHL and bone mass considering all participants (CG and SBSG0 ) (R2 = 0.38; P < .05). CONCLUSION: Appropriate nutrition assistance recovers body composition, reverts the relationship of bone mass and MAT, and mitigates bone loss in SBS. In spite of this, osteoporosis seems to be an early and persistent complication in SBS. Curiously, SBS seems to be a highly vulnerable condition for the development of hepatic steatosis and shows an association between bone mass and IHL.

Short bowel syndrome: influence of nutritional therapy and incretin GLP1 on bone marrow adipose tissue.

Energy deprivation leads to a decrease in white adipose tissue and bone mineral density (BMD), while simultaneously inducing the expansion of marrow adipose tissue (MAT). In short bowel syndrome (SBS), parenteral nutrition mitigates the deterioration of nutritional status, including decreases in MAT. Osteoporosis is, however, a frequent complication of SBS. The objective of our study here was to evaluate the association of fat deposit sites (subcutaneous and visceral adipose tissues: intrahepatic lipid (IHL) and MAT) and the incretin glucagon-like peptide 1 (GLP1) with BMD in individuals with SBS. MAT was negatively correlated with lumbar spine BMD in normal individuals, but not in those in the SBS group, who otherwise showed a positive correlation between MAT and GLP1. In addition, in individuals with SBS, IHL was negatively associated with lumbar spine BMD and positively associated with C-terminal telopeptide of type 1 collagen (a serum biomarker of bone turnover). Caloric maintenance in individuals with SBS, therefore, seems to positively affect the relationship between MAT and BMD, which may be modulated, at least in part, by GLP1.