Chang GQ, Karatayev O, Ahsan R, Gaysinskaya V, Marwil Z, Leibowitz SF. Dietary fat stimulates endogenous enkephalin and dynorphin in the paraventricular nucleus: role of circulating triglycerides. Am J Physiol Endocrinol Metab 292: E561-E570, 2007; doi:10.1152/ajpendo.00087.2006.-The opioid peptides enkephalin (ENK) and dynorphin (DYN), when injected into the hypothalamus, are known to stimulate feeding behavior and preferentially increase the ingestion of a high-fat diet. Studies of another peptide, galanin (GAL), with similar effects on feeding demonstrate that a high-fat diet, in turn, can stimulate the expression of this peptide in the hypothalamus. The present study tested different diets and variable periods of high-vs. low-fat diet consumption to determine whether the opioid peptides respond in a similar manner as GAL. In six experiments, the effects of dietary fat on ENK and DYN were examined in three hypothalamic areas: the paraventricular nucleus (PVN), perifornical hypothalamus (PFH), and arcuate nucleus (ARC). The results demonstrated that the ingestion of a high-fat diet increases gene expression and peptide levels of both ENK and DYN in the hypothalamus. The strongest and most consistent effect is seen in the PVN. In this nucleus, ENK and DYN are increased by 50 -100% after 1 wk, 1 day, 60 min, and even 15 min of high-fat diet consumption. While showing some effect in the PFH, these peptides in the ARC are considerably less responsive, exhibiting no change in response to the briefer periods of diet intake. This effect of dietary fat on PVN opioids can be observed with diets equal in caloric density and palatability and without a change in caloric intake, body weight, fat pad weight, or levels of insulin or leptin. The data reveal a strong and consistent association between these peptides and a rise in circulating levels of triglycerides, supporting a role for these lipids in the fat-induced stimulation of opioid peptides in the PVN, similar to GAL. galanin; opioid peptides; arcuate nucleus; feeding behavior; lipids RECENT EVIDENCE has demonstrated a close relationship between the orexigenic peptide galanin (GAL) and the consumption of a fat-rich diet. When injected into the paraventricular nucleus (PVN), this peptide stimulates feeding behavior in rats, and while having no specific effect on macronutrient preferences, GAL produces its strongest response in animals that prefer fat or are maintained on a fat-rich diet (34,41,65). Moreover, measurements of endogenous GAL reveal a stimulatory effect of acute or chronic high-fat diet consumption on gene expression and peptide levels specifically in the PVN (13,36,52). This supports the existence of a positive feedback loop, whereby a peptide stimulates intake of a diet that, in turn, increases production of this same peptide.The focus of this study is on the endogenous opioid peptides, enkephalin (ENK) and dynorphin (DYN). These peptides, like GAL, are known to increase feeding in a dose-dependent manner, and this response is observed with injection in...

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INTRODUCTION: Mesenteric ischemia (MI) is caused by inadequate blood flow through the mesenteric vessels resulting in ischemic bowel. The most serious cases cause gangrenous bowel, leading to pneumatosis intestinalis (PI) and portal venous gas (PVG), often an ominous sign. CASE DESCRIPTION/METHODS: This is a case of a 63-year-old male who presented to the hospital with hematemesis and severe anemia. After massive transfusion, an EGD revealed actively bleeding gastric ulcers, requiring serial EGDs for successful control of bleeding. A CT revealed gastric distention with thickening of the duodenum and bilateral femoral vein opacities, later confirmed as deep vein thromboses. An IVC filter was subsequently placed, as he was not a candidate for anticoagulation. The patient was subsequently discharged on oral pantoprazole. Of note, there was no history of NSAID use or evidence of H. pylori. Repeat EGD 2 months later noted mild gastritis, but no ulcers were seen. A screening colonoscopy at the time noted only diverticulosis. He was continued on pantoprazole. 3 months later he presented to the hospital with acute onset nausea, vomiting, and diarrhea. A CT revealed PI at the gastric fundus, as well as PVG. An infectious work-up was negative, lactate was normal, and his symptoms resolved quickly. A subsequent repeat CT noted resolution of the PVG and reduction in PI. He represented to the hospital 1 month later again with nausea, vomiting, and diarrhea. A CT noted small bowel dilatation with air fluid levels, PI at the esophagus, stomach, and jejunum, and significant PVG. The initial lactate level was mildly elevated and his symptoms resolved quickly after bowel decompression. A subsequent CTA noted a significant reduction in PVG without evidence of vascular occlusion. A follow up EGD showed diffuse subepithelial hemorrhages without any evidence of recurrent ulcers. A subsequent CTE noted a thrombus above the IVC filter and an evolving hepatic infarction. He was asymptomatic at the time, however, he was admitted to the hospital for anticoagulation. He has since remained on warfarin without any recurrence of symptoms, PI, or PVG. A follow-up CTA showed a full resolution of venous thromboses. DISCUSSION: Previous case reports have described the development of PI and PVG secondary to underlying MI. This case highlights an example of MI secondary to an increase in the resistance of mesenteric blood flow due to venous thromboses. When investigating IP and PVG, underlying venous thromboses should always be considered.

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