2003

MedGenMed. 2003 Aug 7;5(3):20.
Low fasting serum triglyceride level as a precocious marker of autoimmune disorders.
Iannello S, Cavaleri A, Milazzo P, Cantarella S, Belfiore F.
Department of Internal Medicine, University of Catania Medical School, Garibaldi Hospital, Catania, Italy.

The authors recently reported the occurrence of low fasting serum triglyceride (TG) and high free fatty acid (FFA) levels in idiopathic pulmonary fibrosis. TG estimation in diverse groups of patients with autoimmune disease or hyperactive immune response confirmed the occurrence of a similar decrease of TG. In some patients, serum FFA level was also evaluated. TG value in lean and obese patients was compared with that in lean (n = 108) and obese (n = 208) control subjects without autoimmune disease. In patients affected by autoimmune chronic thyroiditis with enhanced concentration of antithyroglobulin antibodies and without thyroidal failure (n = 24), lean and obese patients had reduced TG (-69/%, P < .01 and -52%, P < .0001, respectively). Both lean and obese patients affected by chronic active B or C hepatitis (n = 26), with autoantibodies and without signs of hepatic insufficiency or cirrhosis, presented reduced TG (-57%, P < .01 and -61%, P < .001, respectively). A marked TG decrease (-73%, P < .001) was observed in the lean patients affected by lupus-like syndrome (n = 7). The lean and obese patients with systemic lupus erythematosus or rheumatoid arthritis (n = 11) showed TG decrease (-66%, P < .01 and -55%, P < .05, respectively). In patients affected by anamnestic allergy or atopic dermatitis/asthma (n = 66), both lean and obese, TGs were reduced (-67%, P < .0001 and -62%, P < .001, respectively). In isolated cases of diverse autoimmune diseases (scleroderma, APECED [autoimmune polyendocrinopathy, candidiasis, and ectodermal dystrophy], urticaria or urticarial vasculitis, Reiter or Sjogren syndromes, ulcerative colitis or Crohn's disease, multiple sclerosis or Guillain-Barre syndrome) (n = 14), decreased TG was also observed both in the lean and obese subjects (-59%, P < .01 and -57%, P < .01, respectively). Concerning FFA (n = 69), value in lean patients (n = 22) vs that in lean controls (n = 18) was increased (520 +/- 31 vs 299 +/- 30 mcEq/L, +74%, P < .001), whereas value in obese patients (n = 18) vs that in obese control subjects (n = 11) was decreased (542 +/- 34 vs 774 +/- 62, -30%, P < .01). This opposite behavior of FFA in lean and obese patients needs to be confirmed. Data in this study seem to indicate that low TG value may be a precocious marker of autoimmunity or immune system hyperreactivity.

1997

Endocrinology. 1997 Feb;138(2):734-40
Fasting prevents experimental murine colitis produced by dextran sulfate sodium and decreases interleukin-1 beta and insulin-like growth factor I messenger ribonucleic acid.
Savendahl L, Underwood LE, Haldeman KM, Ulshen MH, Lund PK.
Department of Pediatrics, University of North Carolina, Chapel Hill 27599, USA.

Cytokines and insulin-like growth factors (IGFs) are involved in the induction and/or perpetuation of inflammatory bowel disease. The effect of fasting on inflammatory bowel disease was studied in a mouse experimental model of acute colitis caused by adding dextran sulfate sodium (DSS) to drinking water. Animals were either fed ad libitum or fasted (water only) for 2 days before death. Inflammation and tissue damage, measured as a colitis activity score, were markedly reduced in fasted (2.4 +/- 0.1) compared to fed (5.3 +/- 0.1) DSS animals (P < 0.0001). Colon interleukin-1 beta (IL-1 beta), IGF-I, and tumor necrosis factor-alpha messenger RNAs (mRNAs) were quantified by Northern blot hybridization and expressed as a percentage of mRNA abundance in fed controls. In DSS mice, IL-1 beta mRNA was elevated in the fed group (954 +/- 155%; P < 0.001), but was suppressed in fasted animals (71.1 +/- 11%). IGF-I mRNA also was elevated in fed DSS mice (421 +/- 71%; P < 0.01). This increase was attenuated in fasted DSS mice (202 +/- 17%; P < 0.01 compared to fed DSS mice). Tumor necrosis factor-alpha mRNA was increased in fed DSS mice (162 +/- 15%; P < 0.01), but was not significantly lower in fasted animals. By in situ hybridization, IL-1 beta mRNA was localized to the lamina propria of colonic mucosa in fed DSS animals, but was not detectable in other groups. We conclude that fasting has a protective effect on the progression of acute DSS, induced colitis. This is associated with decreased _expression of IL-1 beta and IGF-I mRNAs in the colon.

2002

Digestion. 2002;65(1):30-4
Effect of fasting on diarrhoea in collagenous colitis.
Bohr J, Jarnerot G, Tysk C, Jones I, Eriksson S.
Department of Medicine, Division of Gastroenterology, Orebro University Hospital, Orebro, Sweden.

BACKGROUND/AIM: Diarrhoea in collagenous colitis has been considered as secretory though the pathophysiology has been studied thoroughly in only a few patients. The result of fasting is one way to distinguish between secretory and osmotic diarrhoea. Our aim was to investigate the effect of fasting on diarrhoea in collagenous colitis. METHODS: Fourteen patients with collagenous colitis were admitted to the hospital for investigation. All were female. Five of these did not have diarrhoea during admission and were excluded. Stools were examined for weight, electrolytes, pH, fat and osmolality during a period on a normal diet and during fasting. RESULTS: During the fasting period the faecal weight was significantly reduced from median 757 (440-3,198) to 191 (22- 2,197) g. The faecal sodium concentration was also reduced, though not significantly, during fasting from median 65 (29-85) to 45 (19-88) mmol/l. The osmotic gaps varied according to the method of calculation applied. CONCLUSIONS: The data indicate that the cause of the diarrhoea in collagenous colitis could be multifactorial. In some patients an osmotic factor dominates and in others a secretory factor, while in some patients a combination of both seems to exist.

2003

Dig Liver Dis. 2003 Jul;35 Suppl 3:S12-6.
Gallbladder motility in obesity, diabetes mellitus and coeliac disease.
Fraquelli M, Pagliarulo M, Colucci A, Paggi S, Conte D.
University of Milan, Milan, Italy.

We reviewed data on gallbladder motility in obesity, diabetes and coeliac disease. In obesity, a condition characterised by increased risk of gallstone(s), decreased gallbladder motility has heterogeneously been reported as a consequence of the different type of meals used to induce gallbladder contraction, characteristics of the population studied, technique used, and proportion of patients with hyperinsulinaemia. Moreover, recent studies have evaluated the effect of dietary restriction on gallbladder motility in obese patients. A two- to three-fold increase in the risk of cholesterol gallstone(s) has been reported in diabetic patients, mainly in relation to obesity and hypertriglyceridaemia. Furthermore, decreased gallbladder motility has been described and attributed to other factors, including underlying autonomic neuropathy, reduced gallbladder sensitivity to cholecystokinin and/or reduced number of cholecystokinin receptors on the gallbladder wall. Impaired gallbladder motility has been reported also in patients with coeliac disease in relation to reduced secretion of enteric hormones and/or decreased gallbladder sensitivity to them. In particular, untreated coeliacs, when compared to controls, showed low postprandial cholecystokinin and increased fasting somatostatin levels. Interestingly, the correlation between fasting somatostatin levels and gallbladder size has clearly been confirmed in patients affected by somatostatinoma or treated with somatostatin or its analogues. Gallbladder motility can be affected by various clinical conditions, such as obesity, diabetes mellitus and coeliac disease.

2000

Aliment Pharmacol Ther 2000 May;14 Suppl 2:51-3
Review: low caloric intake and gall-bladder motor function.
Festi D; Colecchia A; Larocca A; Villanova N; Mazzella G; Petroni ML; Romano F; Roda E.
Department of Medicine and Aging, University G. d'Annunzio, St Annunziata Hospital, Chieti, Italy.

Cholelithiasis is the primary _expression of obesity in the hepatobiliary system. In obese subjects the risk of developing gallstones is increased due to a higher cholesterol saturation of gall-bladder bile. During weight reduction with very low calorie diets (VLCD) the incidence of gallstones increases, but the mechanism for gallstone formation is not completely understood and several pathogenetic mechanisms have been suggested: increased saturation of bile, increased gall-bladder secretion of mucin and calcium, increased presence of prostaglandins and arachidonic acid. Alterations in gall-bladder motility may contribute to gallstone formation, but few studies have addressed the issue of gall-bladder motility during rapid weight loss and its possible role in gallstone formation. VLCD have been associated with a gall-bladder stasis, as a consequence of reduced gall-bladder stimulation by low fat content of the diets. A threshold quantity of fat (10 g) has been documented to obtain efficient gall-bladder emptying. Ursodeoxycholic acid administered during VLCD seems to have a protective role in developing a biliary cholesterol crystals. Gall-bladder emptying was lower in response to low fat meals with respect to relative higher fat meals, before as well as during the VLCD. This may account the possibility of an adaptative response of the gall-bladder motility to a given diet regimen. Adequate fat content of the VLCD may prevent gallstone formation, maintaining adequate gall-bladder motility and may be more economic and physiologically acceptable than administration of a pharmacological agent.

1998

Int J Obes Relat Metab Disord 1998 Jun;22(6):592-600
Gallbladder motility and gallstone formation in obese patients following very low calorie diets. Use it (fat) to lose it (well).
Festi D; Colecchia A; Orsini M; Sangermano A; Sottili S; Simoni P; Mazzella G; Villanova N; Bazzoli F; Lapenna D; Petroni ML; Pavesi S; Neri M; Roda E.
Department of Medicine and Aging, University G D'Annunzio Chieti, Italy.

Dieting obese subjects are at risk of developing gallstones. A gallbladder motor dysfunction could have a pathogenetic role. The principal aim of this study was to evaluate the long term effects of two very low calorie diets differing in fat content on gallbladder emptying and gallstone formation in obese subjects. DESIGN AND SUBJECTS: Gallbladder emptying in response to meals (breakfast, lunch and dinner) in two different diet regimens (3.0 vs 12.2 g of fat/d) was evaluated by ultrasonography in 32 gallstone-free obese patients on different days, before and during (at 45 d intervals) one or two 6-month weight reduction diets (for the first three months: 2.24 MJ (535.2 kcal), 3.0 g fat/d vs 2.415 MJ (577.0 kcal), 12.2 g fat/d; for the second three months, the same low calorie diet of 4.194 MJ (1002 kcal)/d for both groups). In 10 subjects, bile analysis was also performed. RESULTS: Twenty-two (69%) subjects concluded the study, eleven in each group, and a significant weight loss was achieved by all subjects. Gallstones (asymptomatic) developed in 6/11 (54.5%) (P < 0.01) of subjects following the lower fat diet, but in none with the higher fat regimen. In the dieters during the first three months (very low calorie phase) the higher fat meals always induced a significantly greater gallbladder emptying than the lower fat meals. The cholesterol saturation index initially increased significantly and then decreased, without difference between the two groups. CONCLUSION: In the obese during rapid weight loss from a very low calorie diet, a relatively high fat intake could prevent gallstone formation, probably by maintaining an adequate gallbladder emptying, which could counterbalance lithogenic mechanisms acting during weight loss.

1995

Int J Obes Relat Metab Disord. 1995 Aug;19(8):593-5
Gallstone formation in obese women treated by a low-calorie diet.
Spirt BA, Graves LW, Weinstock R, Bartlett SJ, Wadden TA.
State University of New York Health Science Center (Syracuse, NY), Department of Radiology, USA.

This study assessed the incidence of gallstone formation in 47 obese women who consumed a low-calorie diet (LCD) for the first 16 weeks of a 26-week weight loss program. The LCD consisted of four daily servings of a liquid diet combined with an evening meal of a pre-packaged dinner entree and provided approximately 925 kcal/d. Six of the 47 patients (12.8%) displayed gallstones at week 17, as determined by sonography. Five patients were asymptomatic when followed for up to 48 weeks. The sixth, however, reported severe abdominal pain 30 weeks after beginning treatment and required a cholecystectomy. Patients who developed gallstones, as compared with those who did not, had significantly higher baseline triglyceride and total cholesterol levels and had a significantly greater rate of weight loss. Results of this study indicate that an increased risk of gallstones is not limited to very-low-calorie diets and that the incidence of this complication should be assessed in persons who consume popular over-the-counter meal replacement plans.