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A total of 722 surgical cases of Meckel's diverticulum was encountered at the Mayo Clinic from 1906 through 1960. In 560 cases it was an incidental finding in the course of other surgical procedures, while in 162 cases the diverticulum was the specific cause for surgical intervention. The symptomatic diverticula presented in the following manner: persistent omphalomesenteric fistula (8), component of a hernial sac (9), intussusception (15), inflammation (29), intestinal obstruction excluding intussusception (28), hemorrhage (63), and neoplasm (10). The symptoms of diseased diverticulum are not specific to it alone but rather are characteristic of the pathologic process occurring in it. For this reason, Meckel's diverticulum must be considered as a possible cause of any intra-abdominal condition which cannot be readily diagnosed.MECKEL' S DIVERTICULUM is an anatomic entity whose clinical and surgical manage¬ ment has intrigued physicians for more than 150 years. Numerous papers have appeared detailing each of the ways the symptomatic diverticulum makes its presence known. This presentation is an attempt to describe the over-all experience of the Mayo Clinic with this interesting problem.The first recorded description of Meckel's diver¬ ticulum has been attributed to Fabricius Hildanus ' in 1598. In the ensuing years the literature on this subject was enriched by the writings of Lavater,2 Ruysch,:1 and Littre '; however, it remained for Meckel5 to establish this condition on sound ana¬ tomic and embryologie grounds in numerous arti¬ cles appearing between 1808 and 1820.The omphalomesenteric duct connects the yolk sac with the intestinal tract at the junction of the foregut and hindgut during early embryonic life and is normally completely obliterated by the fifth to seventh week of gestation. Failure of complete obliteration may result in an omphalomesenteric fistula, Meckel's diverticulum, an enterocyst, or a fibrous band running from the small intestine to either the adjacent bowel or the umbilicus. Originally, paired omphalomesenteric arteries and veins were present. The left artery and right vein normally are obliterated, but the right artery is incorporated into the superior mesenteric artery while the left vein forms part of the portal vein.All of the surgical cases of Meckel's diverticulum encountered from 1906 through 1960 at the Mayo Clinic were reviewed and classified into 2 groups depending on whether the diverticulum was an incidental surgical finding or whether it was the seat of surgical disease. The latter category was then subdivided into the various pathologic condi¬ tions encountered at operation. A total of 722 cases was reviewed; these form the basis of this paper. Incidental Surgical Finding.-A total of 560 diverticula in this series comprised the incidental sur¬ gical findings, 402 being excised and 158 being left in situ. The main reason for leaving the diverticu¬ lum in place was that wide-mouthed diverticula were not deemed to be potential sources of danger, and thus their removal would add...

The recruitment of new fat cells through adipogenesis may prevent the development of obesity-related comorbidities. However, adipogenic capacity is markedly reduced in mature adults. This study examined how initiation of high-fat feeding at different phases of adulthood modified adipose tissue (AT) morphology and obesity phenotype in obese and diabetic Zucker Diabetic Sprague Dawley (ZDSD) rats. For this, rodents were provided high-fat diet (HFD) beginning at 63, 84, or 112 d after parturition until termination (n = 6). At termination, ZDSD rats fed HFD beginning at 63 d after parturition (early adulthood) exhibited greater body fat and lower lean mass without significant changes to energy intake or body weight. Moreover, early high fat feeding increased adipocyte size and number, whereas these effects were absent at 84 or 112 d after parturition. At 126 d after parturition, there were no detectable transcript differences in PPARγ or C/EBPα. However, rodents provided HFD in early adolescence exhibited lower expression of canonical Wnt signaling intermediates. Corresponding with these changes was a marked reduction in AT-specific inflammation, as well as overall improvement in systemic glucose, lipid, and inflammatory homeostasis. Taken together, these data indicate that dietary regulation of adipocyte recruitment in adolescence may represent a major determinant of obesity phenotype.

This study examined the ability of flax-based ingredients to attenuate nonalcoholic fatty liver disease ( NAFLD: ) in aged laying hens-a novel and more physiologically relevant model of human disease. Our results showed only hens supplemented with whole flaxseed ( WFX: ) reduced steatosis and hepatocellular ballooning. Serum AST was also reduced in hens provided WFX and defatted flaxseed meal ( DFM: ). Hepatic ω-3 PUFA enrichment was improved with supplementation of WFX, DFM, and flaxseed oil ( FXO: ). However, this effect was more evident in the WFX group. In contrast, transcript abundance of genes linked to NAFLD were predominantly modified with FXO supplementation. Taken together, our data indicate a potential synergistic relationship between the fatty acid and lignan content in flaxseed which attenuated the progression of NAFLD in aged laying hens. Although more research is necessary, these findings demonstrate the potential use of whole flaxseed for the treatment and prevention of NAFLD in humans.

We have previously shown that soy protein isolate (SPI) with intact phytoestrogen content prevented obesity-related dysfunction. Recent data have suggested that soy ingredients may act as regulators of adipogenic programming in adipose tissue (AT) and liver. Thus, the current study was undertaken to determine whether the beneficial effects of SPI are linked to changes in adipogenic regulators, such as the Wnt signaling cascade. For this, lean (LZR) and obese Zucker (OZR) rats were provided isocaloric and isonitrogenous diets containing SPI, sodium caseinate, or dairy whey protein for 17 weeks. At termination, SPI increased body weight and total adiposity in rodents, which corresponded with an increase in both adipocyte size and number. Furthermore, markers of inflammation, hypercholesterolemia, and hepatic steatosis were all reduced in OZR rats provided SPI. Transcript abundance of several canonical and noncanonical Wnt signaling intermediates in liver, but not AT, was distinctly modified by SPI. Collectively, these data confirm the protective SPI attenuated obesity-related metabolic dysfunction conceivably through regulation of adipogenic programming, as evident by changes in AT morphology and hepatic Wnt signaling. Collectively, this study confirmed the potential utilization of soy protein and its bioactive ingredients for prevention and treatment of obesity-related comorbidities.

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