Changes in Plasma Fatty Acid Profile in Japanese Patients with Chronic Pancreatitis

Abstract

The serum zinc, prealbumin, retinol-binding protein and carotene concentrations and the plasma fatty acid composition were determined to assess the nutritional condition of 24 patients with chronic pancreatitis compared with that of 20 healthy controls. The daily food intake and faecal fat excretion of the two groups were also measured. In the chronic pancreatitis group, the calorie and fat intakes were significantly lower than those of the controls. Serum levels of zinc, prealbumin and carotene were also significantly lower than those of the controls. Percentages of plasma linoleic and arachidonic acids were low, while percentages of palmitoleic acid, eicosapentaenoic acid and docosahexaenoic acid were high. Fish oil intake correlated negatively with plasma linoleic acid concentration (P < 0.05). The above results indicate that the relatively high intake of fish oil and the relatively low intake of dietary fat in Japanese patients with chronic pancreatitis with a mild degree of steatorrhoea results in an abnormally low plasma level of linoleic acid.

Fatty Acid Composition of Plasma Lipid Classes in Chronic Alcoholic Pancreatitis

“…In parallel with the data of Nakamura et al [12] we also found significantly lower arachidonic acid values in patients with CP than in controls. The significant reduction of plasma arachidonic acid in CP may be explained in part by the reduced availability of the parent essential fatty acid, linoleic acid.…”

“…Furthermore, overexpression of cyclooxygenase 2, the enzyme catalyzing a critical step in the conversion of arachidonic acid to prostaglandins, was described in CP patients [15] and may contribute to an enhanced arachidonic acid expenditure in CP. We did not see higher EPA and DHA values in patients with CP as the Japanese authors did in their study [12]; however, values of total n–3 LCPUFA were significantly higher, whereas values of n–6 LCPUFA significantly lower in patients with CP than in controls in the present study. Consequently, the ratio of n–3 to n–6 LCPUFA (a surrogate parameter indicating the availability of precursors for the synthesis of eicosanoids with less as opposed to more pronounced inflammatory effect) was by no means lower in the patients with CP than in the healthy controls.…”

“…We are aware of two studies addressing the question of fatty acid profile in CP. Reduced contribution of linoleic and arachidonic acids, but an enhanced contribution of palmitoleic acid, EPA and DHA was found in plasma fatty acid in Japanese patients with CP than in healthy controls [12]. Quilliot et al [13] included patients with CP and type 1 diabetes mellitus, patients with CP but without diabetes, patients with diabetes but without CP and controls into their study on fatty acid composition of LDL lipids.…”

“…Animal data raised the idea of a beneficial potential for n–3 LCPUFA supplementation in CP; however, the very few human observational data on LCPUFA in CP are controversial. A non-diminished, but enhanced percentage contribution of EPA and DHA to the plasma fatty acid profile was reported in patients with CP as compared to healthy controls in one study [12], and no difference was seen in the contribution of LCPUFA to LDL lipids between patients with CP and controls in another study [13]. …”

An enteral therapy containing medium-chain triglycerides and hydrolyzed peptides reduces postprandial pain associated with chronic pancreatitis

“…Although the mechanism by which pain occurs in patients with chronic pancreatitis is not completely understood, CCK has been postulated to play a role through hyperstimulation of exocrine pancreatic secretion as well as increasing pancreatic ductal pressures [10]. Several studies have examined CCK levels in patients with chronic pancreatitis, with some showing increased basal and postprandial levels [11][12][13], while others found no difference [14][15][16][17][18]. Garces et al [19] found that basal as well as meal-stimulated plasma CCK levels were higher in chronic pancreatitis patients with pain as compared with those without pain.…”