Effects of zinc deficiency and castration on fatty acid composition and desaturation in rats

Clejan, Sanda; Castro‐Magana, Mariano; Collipp, P.J.; Jonas, Ernesto; Maddaiah, V.T.

doi:10.1007/bf02535092

Cited by 86 publications

(37 citation statements)

References 16 publications

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“…In support of this suggestion is the very stable repartition in the phospholipids between endogenous (saturated and mono-unsaturated fatty acids) and exogenous fatty acids (n-6 and n-3 families) shown in Tables 3 to 5. These results agree with those of Clejan et al [4].…”

Section: Discussionsupporting

confidence: 94%

See 1 more Smart Citation

Effects of Gamma-Linolenic Acid Supplementation on Lipid Composition of Liver Microsomal Membranes

DIB¹,

CLAVEL²,

CARREAU³

1989

J. Clin. Biochem. Nutr.

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Section: Discussionsupporting

confidence: 94%

“…is required for the activity of 46 desaturase, a microsomal enzyme that converts linoleic acid into gamma-linolenic acid and that it may be one of the important factors in the cause of essential fatty acid deficiency [4].…”

mentioning

confidence: 99%

Effects of Gamma-Linolenic Acid Supplementation on Lipid Composition of Liver Microsomal Membranes

DIB¹,

CLAVEL²,

CARREAU³

1989

J. Clin. Biochem. Nutr.

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“…Desaturase activities could also be affected in diabetes mellitus and be dependent on insulin (el Boustani et al, 1989). Furthermore, it has been suggested that zinc and selenium could play a role in the desaturation of n-3 and n-6 polyunsaturated fatty acids (Clejan et al, 1982;Infante, 1986;Celik et al, 1999). To this end, we have already shown (Quilliot et al, 2001) that the plasma zinc concentration was below normal in chronic pancreatitis patients, and that plasma selenium concentra-tions were lower in chronic pancreatitis patients than in healthy controls.…”

Section: Introductionmentioning

confidence: 86%

Fatty acid abnormalities in chronic pancreatitis: effect of concomitant diabetes mellitus

et al. 2003

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Objective: Patients with chronic pancreatitis suffer from malabsorption and nutritional deficiencies. However there is little data available concerning the fatty acid profile in chronic pancreatitis. Diabetes mellitus, a common complication of this disease, could interfere with the metabolism of fatty acids. Subjects: We therefore compared the fatty acid composition of LDL from four groups of male patients with (a) chronic pancreatitis without diabetes (ND-CP; n ¼ 12), (b) diabetes secondary to chronic pancreatitis and insulin-treated (CP-D; n ¼ 35); (c) type 1 diabetes (n ¼ 25); and (d) controls (n ¼ 20). Results: The patients in both groups of chronic pancreatitis (ND-CP and CP-D) had lower mean values for linoleic acid than that seen in the type 1 DM and control groups, whereas monounsaturated fatty acids (MUFA; 18 : 1(n-9) and (16 : 1(n-7)) were significantly increased in these two groups (ND-CP and CP-D). Docosa-hexaenoic-acid (22 : 6(n-3)) was significantly decreased in the CP-D group (P > 0.05), a response that could be explained by the effects of diabetes mellitus and by selenium deficiency. In this way, diabetes was associated with a decrease in the docosa-hexaenoic-acid (22 : 6(n-3); r ¼ 0.30, P ¼ 0.005), and selenium was correlated with DHA (r ¼ 0.28, P ¼ 0.029) and with the 22 : 6(n-3)=20 : 5(n-3) ratio (evaluating the delta 4 desaturation); r ¼ 0.31, P ¼ 0.022), independently of the diabetes effect. Selenium was negatively correlated with 20 : 4(n-6)/ 20 : 3(n-6) ratio (evaluating the delta 5 desaturase; r ¼ -0.30; P ¼ 0.025). These results suggest that these two factors may have a role in the regulation of the desaturation process. If we consider that a ratio of 16 : 1(n-7)=18 : 2(n-6) greater than 0.086 in plasma indicates an EFAn-6 deficiency, 40% of our CP patients, 57.6% of CP-D patients and 13.6% of type 1 DM patients were involved. Conclusions: The consequences of these deficiencies are not evaluated in this disease. However, correction of the fundamental deficiencies in essential fatty acids and in selenium seems desirable in chronic pancreatitis.

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“…The physicochemical and transport properties of both the brush border and basolateral membranes can vary with fatty acyl chain composition, cholesterol and phospholipid head group content [9,11]. In turn, these components, and hence structural and metabolic activities of enterocytes, can be influenced by fasting and dietary manipulation [9,10,[12][13][14][15]. While there has been interest in the possible interaction of vitamin A status and membranes for many years [16][17][18][19], and young rats given large doses of vitamin A have been found to have greater total intestinal lipid content and monoglycerides than controls [20,21], we are not aware of any studies conducted to investigate intestinal epithelial lipid composition in vitamin A deficiency.…”

Section: Discussionmentioning

confidence: 99%

“…Although no studies have examined the effect of protein energy malnutrition on intestinal fatty acid profile, malnourished rabbits have an altered intestinal microvillous membrane lipid composition [13], and short-term fasting in rats has been found to modify the fatty acid profile of intestinal microsomes [12]. Furthermore, by feeding the same diet to all groups of rats, we have also controlled for the effects of any other nutrients which may influence intestinal mucosal fatty acid composition [9,10,12,14,15].…”

Section: Discussionmentioning

confidence: 99%

Vitamin A Deficiency Changes Jejunal Mucosal Fatty Acid Profile in Rats

Warden

Noltorp

Bell

et al. 2002

J. Clin. Biochem. Nutr.

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SummaryChanges in intestinal epithelial integrity have been postulated to explain the association between vitamin A status and diarrhoeal disease in children living in areas where vitamin A deficiency is a major public health problem. Fatty acids are an integral component of normal enterocyte structure, and changes to their profile in the intestinal mucosa may impact on the efficacy of the mucosal barrier. The aim of this study therefore was to determine the effect of vitamin A deficiency on intestinal mucosal fatty acid profile. Weanling male specific pathogen free rats were maintained on a vitamin A deficient diet for either 40-42 (subclinical deficiency) or 60-63 days (clinical deficiency), and compared with rats pair fed or allowed free access to the same diet, but supplemented with vitamin A (vitamin A sufficient). Fatty acid profile of jejunal mucosal homogenates was determined using gas chromatography. While subclinically vitamin A deficient rats had only minor differences in fatty acid profile as compared with pair fed and vitamin A sufficient rats, there were marked differences in a number of fatty acids in the clinically vitamin A deficient rats. Clinically vitamin A deficient rats had more arachidonic acid (C20:4n-6) than pair fed rats, and less linoleic acid (C 18:2n-6) than both pair fed and vitamin A sufficient rats. These findings suggest that vitamin A deficiency modifies intestinal mucosal fatty acid composition such that there is an increase in proinflammatory eicosanoid precursors. This may contribute towards our understanding of a biological mechanism of the epidemiological association between vitamin A status and diarrhoeal disease.

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Effects of zinc deficiency and castration on fatty acid composition and desaturation in rats

Cited by 86 publications

References 16 publications

Effects of Gamma-Linolenic Acid Supplementation on Lipid Composition of Liver Microsomal Membranes

Effects of Gamma-Linolenic Acid Supplementation on Lipid Composition of Liver Microsomal Membranes

Fatty acid abnormalities in chronic pancreatitis: effect of concomitant diabetes mellitus

Vitamin A Deficiency Changes Jejunal Mucosal Fatty Acid Profile in Rats

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