Neuroendocrine neoplasms (NENs) are derived from neuroendocrine cell system and can have benign or malignant characteristics. They are rare tumors, but have been increasing in incidence over the past 40 years. Patients with NENs may develop symptoms due to primary tumor invasion, metastasis, or from secretion of hormonally active tumor substances. Multiple imaging modalities are used for diagnosis and staging, including specialty scans such as 111In pentetreotide (Octreoscan) and 68Gallium-DOTATATE, along with endoscopy, endoscopic ultrasound, and biochemical marker testing. Treatment involves both surgical approach, for both primary and metastatic lesions, as well as medical management for symptom management and disease progression. This article will review the current clinical knowledge regarding the diagnosis, treatment, and prognosis of these fascinating neoplasms and the associated hormonal syndromes.

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The neurobiological mechanisms that mediate psychiatric comorbidities associated with metabolic disorders such as obesity, metabolic syndrome and diabetes remain obscure. High fructose corn syrup (HFCS) is widely used in beverages and is often included in food products with moderate or high fat content that have been linked to many serious health issues including diabetes and obesity. However, the impact of such foods on the brain has not been fully characterized. Here, we evaluated the effects of long-term consumption of a HFCS-Moderate Fat diet (HFCS-MFD) on behavior, neuronal signal transduction, gut microbiota, and serum metabolomic profile in mice to better understand how its consumption and resulting obesity and metabolic alterations relate to behavioral dysfunction. Mice fed HFCS-MFD for 16 weeks displayed enhanced anxiogenesis, increased behavioral despair, and impaired social interactions. Furthermore, the HFCS-MFD induced gut microbiota dysbiosis and lowered serum levels of serotonin and its tryptophan-based precursors. Importantly, the HFCS-MFD altered neuronal signaling in the ventral striatum including reduced inhibitory phosphorylation of glycogen synthase kinase 3β (GSK3β), increased expression of ΔFosB, increased Cdk5-dependent phosphorylation of DARPP-32, and reduced PKA-dependent phosphorylation of the GluR1 subunit of the AMPA receptor. These findings suggest that HFCS-MFD-induced changes in the gut microbiota and neuroactive metabolites may contribute to maladaptive alterations in ventral striatal function that underlie neurobehavioral impairment. While future studies are essential to further evaluate the interplay between these factors in obesity and metabolic syndrome-associated behavioral comorbidities, these data underscore the important role of peripheral-CNS interactions in diet-induced behavioral and brain function. This study also highlights the clinical need to address neurobehavioral comorbidities associated with obesity and metabolic syndrome.

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