The outcomes of laparoscopic omentum-preserving gastrectomy compared to open surgery with omentectomy in gastric cancer patients: a propensity score matched study of 249 UICC stage 0-IV gastric cancer patients.

BACKGROUND: We performed a propensity score matched study comparing patients' short- and long-term results after laparoscopic omentum-preserving gastrectomy and open surgery with omentectomy with UICC stages 0-IV. METHODS: Between 2015 and 2022, 311 patients with gastric cancer underwent surgery at the University Clinical Centre Maribor. Of these, 249 met the inclusion criteria and 198 were included in the study group after PSM. RESULTS: Patients in both groups were well-balanced in demographic and pathological characteristics after PSM. There was no significant difference in the 5-year survival between groups (LAP: 62.2% vs. OPN: 54.4%; p = 0.950). The Cox regression model identified UICC stage and age as significant predictors for survival. In both groups, peritoneal dissemination was the most common site of recurrence. The multivariate analysis identified the UICC stage as a significant predictor for peritoneal recurrence, while omental preservation was not associated with a higher risk of peritoneal dissemination. Omentum preservation was not associated with more intestinal obstruction. Patients in the LAP group had significantly shorter hospital stays (LAP: 9(6) vs. OPN: 10(5); p = 0.009), less postoperative morbidity (LAP: 17% vs. OPN: 23.4%; p = 0.009), and significantly more extracted LNs per operation compared to open surgery (LAP: 31 ± 11 LNs vs. OPN: 25 ± 12 LNs; p = 0.002). CONCLUSION: Based on our results, we recommend the use of laparoscopic omentum-preserving gastrectomy in patients with early and advanced gastric cancer.

Insulin receptor activation in the nucleus accumbens reflects nutritive value of a recently ingested meal.

With respect to feeding, insulin is typically thought of as a satiety hormone, acting in the hypothalamus to limit ingestive behavior. However, accumulating evidence suggests that insulin also has the ability to alter dopamine release in the striatum and influence food preferences. With increased access to high calorie foods, Western societies have a high prevalence of obesity, accompanied by insulin insensitivity. Little is known about how insulin is trafficked into the brain following food consumption and whether insulin insensitivity in the periphery is mirrored in the central nervous system. We investigated insulin receptor activation in the ventral striatum of rats receiving water or 16% glucose either orally or intragastrically. We also investigated whether glucose-induced insulin receptor activation was altered in food-restricted (FR) or diet-induced obesity (OB) rat models. Lastly, we examined whether insulin plays a significant role in flavor-nutrient preference learning. Glucose intake stimulated a rapid increase in insulin receptor activity in the ventral striatum of FR and ad libitum (AL) fed rats, but not OB rats. Similarly, both AL and FR, but not OB rats demonstrated significant flavor-nutrient preferences. However AL rats receiving brief inhibition of insulin activity during conditioning failed to acquire a significant flavor-nutrient preference. These findings suggest that impaired insulin receptor activation in the ventral striatum may result in inaccurate valuation of nutritive foods, which could lead to overconsumption of food or the selection of foods that don't accurately meet the body's current physiological needs.

Episodic sucrose intake during food restriction increases synaptic abundance of AMPA receptors in nucleus accumbens and augments intake of sucrose following restoration of ad libitum feeding.

Weight-loss dieting often leads to loss of control, rebound weight gain, and is a risk factor for binge pathology. Based on findings that food restriction (FR) upregulates sucrose-induced trafficking of glutamatergic AMPA receptors to the nucleus accumbens (NAc) postsynaptic density (PSD), this study was an initial test of the hypothesis that episodic "breakthrough" intake of forbidden food during dieting interacts with upregulated mechanisms of synaptic plasticity to increase reward-driven feeding. Ad libitum (AL) fed and FR subjects consumed a limited amount of 10% sucrose, or had access to water, every other day for 10 occasions. Beginning three weeks after return of FR rats to AL feeding, when 24-h chow intake and rate of body weight gain had normalized, subjects with a history of sucrose intake during FR consumed more sucrose during a four week intermittent access protocol than the two AL groups and the group that had access to water during FR. In an experiment that substituted noncontingent administration of d-amphetamine for sucrose, FR subjects displayed an enhanced locomotor response during active FR but a blunted response, relative to AL subjects, during recovery from FR. This result suggests that the enduring increase in sucrose consumption is unlikely to be explained by residual enhancing effects of FR on dopamine signaling. In a biochemical experiment which paralleled the sucrose behavioral experiment, rats with a history of sucrose intake during FR displayed increased abundance of pSer845-GluA1, GluA2, and GluA3 in the NAc PSD relative to rats with a history of FR without sucrose access and rats that had been AL throughout, whether they had a history of episodic sucrose intake or not. A history of FR, with or without a history of sucrose intake, was associated with increased abundance of GluA1. A terminal 15-min bout of sucrose intake produced a further increase in pSer845-GluA1 and GluA2 in subjects with a history of sucrose intake during FR. Generally, neither a history of sucrose intake nor a terminal bout of sucrose intake affected AMPA receptor abundance in the NAc PSD of AL subjects. Together, these results are consistent with the hypothesis, but the functional contribution of increased synaptic incorporation of AMPA receptors remains to be established.