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Stumvoll, M.

Publications and source records attributed to Stumvoll, M..

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Neuroanatomical correlates of food addiction and obesity in the general population

The food addiction model suggests neurobiological similarities between substance-related and addictive disorders and obesity. While structural brain differences have been consistently reported in these conditions, little is known about the neuroanatomical correlates of food addiction. We therefore assessed whether food addiction, assessed with the Yale Food Addiction Scale (YFAS), related to obesity, personality and brain structure in a large population-based sample (n=625; 20-59 years old, 45% women). A higher YFAS symptom score correlated with obesity and disinhibited eating. In a whole-brain analysis, YFAS symptom score was not associated with cortical thickness nor subcortical gray matter volumes. Higher body mass index (BMI) correlated with reduced thickness of (pre)frontal, temporal and occipital cortex. Bayes factor analysis suggested that BMI and - to a smaller extent - YFAS symptom score contributed independently to right lateral orbitofrontal cortex thickness. Our study shows that food addiction is not associated with neuroanatomical differences in a large population-based sample, and does not account for the major part of obesity-associated gray matter alterations. Yet, food addiction might explain additional variance in orbitofrontal cortex, a hub area of the reward network. Longitudinal studies implementing both anatomical and functional MRI could further disentangle the neural mechanisms of addictive eating behaviors.

neuroscience

Widely used commercial ELISA for human Zonulin reacts with Complement C3 rather than pre-Haptoglobin 2

BACKGROUNDThere is increasing evidence for the role of impaired intestinal permeability in obesity and associated metabolic diseases. Zonulin is an established serum marker for intestinal permeability and identical to pre-haptoglobin2. Here, we aimed to investigate the relationship between circulating zonulin and metabolic traits related to obesity.\n\nMETHODSSerum zonulin was measured by using a widely used commercial ELISA kit in 376 subjects from the metabolically well-characterized cohort of Sorbs from Germany. In addition, haptoglobin genotype was determined in DNA samples from all study subjects.\n\nRESULTSAs zonulin concentrations did not correlate to the haptoglobin genotypes, we investigated the specificity of the zonulin ELISA assay using antibody capture experiments, mass spectrometry and Western blot analysis. Using serum samples that gave the highest or lowest ELISA signals, we detected several proteins that are likely to be captured by the antibody in the present kit. However, none of these proteins corresponds to pre-haptoglobin2. We used increasing concentrations of recombinant pre-haptoglobin 2 and complement C3 as one of the representative captured proteins and the ELISA kit did not detect either. Western blot analysis using both the polyclonal antibodies used in this kit and monoclonal antibodies rose against zonulin showed a similar protein recognition pattern but with different intensity of detection. The protein(s) measured using the ELISA kit was (were) significantly increased in patients with diabetes and obesity and correlated strongly with markers of the lipid and glucose metabolism. Combining mass spectrometry and Western blot analysis using the polyclonal antibodies used in the ELISA kit, we identified properdin as another member of the zonulin family.\n\nCONCLUSIONSOur study suggests that the zonulin ELISA does not recognize pre-haptoglobin 2, rather structural (and possibly functional) analogue proteins belonging to the mannose-associated serine protease family, with properdin being the most likely possible candidate.

molecular biology