Dataset Information

Differences in brain responses between lean and obese women to a sweetened drink.

ABSTRACT: Ingestion of sweet food is driven by central reward circuits and restrained by endocrine and neurocrine satiety signals. The specific influence of sucrose intake on central affective and reward circuitry and alterations of these mechanisms in the obese are incompletely understood. For this, we hypothesized that (i) similar brain regions are engaged by the stimulation of sweet taste receptors by sucrose and by non-nutrient sweeteners and (ii) during visual food-related cues, obese subjects show greater brain responses to sucrose compared with lean controls.In a double-blind, crossover design, 10 obese and 10 lean healthy females received a sucrose or a non-nutrient sweetened beverage prior to viewing food or neutral images. BOLD signal was measured using a 1.5 Tesla MRI scanner.Viewing food images after ingestion of either drink was associated with engagement of similar brain regions (amygdala, hippocampus, thalamus, anterior insula). Obese differed from lean subjects in behavioral and brain responses rating both beverages as less tasteful and satisfying, yet demonstrating greater brain responses. Obese subjects also showed engagement of an additional brain network (including anterior insula, anterior cingulate, hippocampus, and amygdala) only after sucrose ingestion.Obese subjects had a reduced behavioral hedonic response, yet a greater engagement of affective brain networks, particularly after sucrose ingestion, suggesting that in obese subjects, lingual and gut-derived signaling generate less central hedonic effects than food-related memories in response to visual cues, analogous to response patterns implicated in food addiction.

SUBMITTER: Connolly L

PROVIDER: S-EPMC4114731 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature

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Differences in brain responses between lean and obese women to a sweetened drink.

Connolly L L Coveleskie K K Kilpatrick L A LA Labus J S JS Ebrat B B Stains J J Jiang Z Z Tillisch K K Raybould H E HE Mayer E A EA

Neurogastroenterology and motility 20130409 7

<h4>Background</h4>Ingestion of sweet food is driven by central reward circuits and restrained by endocrine and neurocrine satiety signals. The specific influence of sucrose intake on central affective and reward circuitry and alterations of these mechanisms in the obese are incompletely understood. For this, we hypothesized that (i) similar brain regions are engaged by the stimulation of sweet taste receptors by sucrose and by non-nutrient sweeteners and (ii) during visual food-related cues, ob ...[more]

PMID: 23566308

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Project description:PurposeObesity is characterized by chronic inflammation that may contribute to insulin resistance and promote type 2 diabetes. We have investigated whether inflammatory responses to glycemic and insulinemic variations are altered in obese individuals.MethodsEight obese and eight lean individuals without diabetes had undergone hyperinsulinemic-euglycemic-hypoglycemic and hyperglycemic clamps in a previous study. Using Proximity Extension Assay, 92 inflammatory markers were analyzed from plasma samples at fasting, hyperinsulinemia-euglycemia, hypoglycemia and hyperglycemia.ResultsIn all participants, hyperinsulinemia, hypoglycemia and hyperglycemia led to reductions of 11, 19 and 62 out of the 70 fully evaluable biomarkers, respectively. FGF-21 increased during both hypoglycemia and hyperglycemia while IL-6 and IL-10 increased during hypoglycemia. In obese vs lean participants, Oncostatin-M, Caspase-8 and 4E-BP1 were more markedly suppressed during hypoglycemia, whereas VEGF-A was more markedly suppressed during hyperglycemia. BMI correlated inversely with changes of PD-L1 and CD40 during hyperinsulinemia, Oncostatin-M, TNFSF14, FGF-21 and 4EBP-1 during hypoglycemia and CCL23, VEGF-A and CDCP1 during hyperglycemia (Rho ≤ -0.50). HbA1c correlated positively with changes of MCP-2 and IL-15-RA during hyperinsulinemia (Rho ≥ 0.51) and inversely with changes of CXCL1, MMP-1 and Axin-1 during hypoglycemia (Rho ≤ -0.55). M-value correlated positively with changes of IL-12B and VEGF-A during hyperglycemia (Rho ≥ 0.51). Results above were significant (p < 0.05).ConclusionOverall, hyperinsulinemia, hypo- and hyperglycemia led to suppression of several inflammatory markers and this tended to be more marked in individuals with obesity, insulin resistance and dysglycemia. Thus, acute glycemic or insulinemic variations do not seem to potentiate possible inflammatory pathways in the development of insulin resistance and disturbed glucose metabolism.

Dataset Information

Differences in brain responses between lean and obese women to a sweetened drink.

Publications

Differences in brain responses between lean and obese women to a sweetened drink.

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