Disease relevance of Dihomo-gamma-linolenic acid

• Dihomo-gamma-linolenic acid as the endogenous protective agent for myocardial infarction [1].
• In incubations of E. coli supernatants with arachidonic acid, 5-hydroxy-7,9,11,14-eicosatetraenoic acid and leukotriene A4 were formed, while incubation with 8,11,14-eicosatrienoic acid gave 8-hydroxy-9,11,14-eicosatrienoic acid [2].
• There were significant differences in the levels of liver fatty acids between SIDS and non-SIDS infants in the age group 1 to 6 months, notably in that the fatty acids of the SIDS infants appeared to have lower levels of dihomo-gamma-linolenic acid, which is the precursor of the "1-series" prostaglandins [3].
• Dihomo-gamma-linolenic acid, prostaglandins and dyskinesias [4].
• Dihomo-gamma-linolenic acid reverses hypertension induced in rats by diets rich in saturated fat [5].

Psychiatry related information on Dihomo-gamma-linolenic acid

• After adjusting for age, gender, smoking, alcohol drinking, sports activity, and non-FA dietary factors, the incidence of CHD was significantly and positively associated with the proportion of dihomo-gamma-linolenic acid but inversely associated with arachiadonic acid [6].

High impact information on Dihomo-gamma-linolenic acid

• In a logistic model, a high proportion of dihomo-gamma-linolenic acid remained a significant contributor to the development of diabetes, along with the height of the insulin index, the blood glucose concentration at 60 min, and the fasting insulin concentration [7].
• Suppression of human synovial cell proliferation by dihomo-gamma-linolenic acid [8].
• Expression of this ORF in mouse fibroblast cells demonstrated that the encoded protein was a Delta(5)-desaturase, as determined by the conversion of dihomo-gamma-linolenic acid (C(20:3,n-6)) into arachidonic acid (C(20:4,n-6)) [9].
• In the GLA group, a significant increase in the levels of dihomo-gamma-linolenic acid (20:3omega6) was observed in plasma and membranes, together with a parallel decrease in the 20:4/20:3omega6 ratio after supplementation [10].
• Prolactin and zinc effects on rat vascular reactivity: possible relationship to dihomo-gamma-linolenic acid and to prostaglandin synthesis [11].

Chemical compound and disease context of Dihomo-gamma-linolenic acid

• HPA is a stronger inhibitor of the conversion of alpha-linoleic acid and dihomo-gamma-linolenic acid to arachidonic acid (AA) in hepatoma cells than are EPA, DHA, and AA [12].
• Immunological and biochemical alterations in atopic dermatitis have been attributed to a deficient conversion of omega-6 fatty acids (i.e. linoleic acid, gamma-linolenic acid, and dihomo-gamma-linolenic acid) to prostaglandin (PG) E1 [13].
• In red blood cells dihomo-gamma-linolenic acid (20:3n-6) was reduced in eczema patients, as compared with controls [14].
• This study has shown that hypertension induced in rats by a diet rich in saturated fat (16% coconut oil, 4% palmitic acid by weight) is reversed by the addition of the essential fatty acid, dihomo-gamma-linolenic acid (DHLA), at 5.0% but not at 0.5% of dietary energy [5].
• RESULTS: Even though pretreatment with linoleic acid and dihomo-gamma-linolenic acid and simultaneous treatment with linoleic acid, gamma-linolenic acid, and dihomo-gamma-linolenic acid did not prevent the development of diabetes mellitus, the severity of diabetes was much less [15].

Biological context of Dihomo-gamma-linolenic acid

• In contrast, the increased proportion of DGLA (precursor of the vasorelaxant and anticoagulant prostaglandin E(1)) at term is more consistent with a profile favoring optimal blood flow to nourish the fetal growth spurt [16].
• Potent inhibition of human platelet aggregation and mitogen release was also seen with dihomo-gamma-linolenic acid (8,11,14-eicosatrienoic acid 20:3 omega 6), whose levels are reportedly elevated in Eskimos subsisting on marine diets [17].
• A diet providing a large amount of linoleic acid (14% of the total caloric intake) resulted in low levels of dihomo-gamma-linolenic acid (C20:3 omega 6) and arachidonic acid (C20:4 omega 6) in serum phospholipids and cholesteryl esters [18].
• We suggest that a relative deficiency in dihomo-gamma-linolenic acid-derived prostaglandin E1 is the major etiologic factor for diminished T cell maturation postpartum [19].
• Administration of structurally similar fatty acids, dihomo-gamma-linolenic acid, and 8,14,17-eicosatrienoic acid, produced vasoconstriction and decreased myocardial tension without affecting heart rate or the output of prostaglandins [20].

Anatomical context of Dihomo-gamma-linolenic acid

• EPA and the elongation product of GLA, dihomo-gamma-linolenic acid (DGLA) levels in neutrophil glycerolipids increased significantly during the 3-wk supplementation period [21].
• The effect of EPO (10, 20 and 30 ml/day) and SO (20 ml/day) for 4 months on the deposition of linoleic acid metabolites in adipose tissue of 4 groups of 6-9 men with low adipose dihomo-gamma-linolenic acid was examined [22].
• Using 1-acyl-LPC as the acceptor, all the intracellular membrane preparations showed transferase preference for the CoA ester of 8,11,14-eicosatrienoic acid [23].
• The effects of 8,11,14-eicosatrienoic acid [20:3 (n--6)], 5,8,11,14-eicosatetraenoic acid [20:4 (n--6)], and alpha-tocopherol (vitamin E) on the morphology of smooth muscle cells from the guinea pig were studied in tissue culture [24].
• The levels of dihomo-gamma-linolenic acid (DHLA) and GLA showed a significant dose-related increase in liver, erythrocyte and aorta phospholipids [25].

Associations of Dihomo-gamma-linolenic acid with other chemical compounds

• The polyunsaturated fatty acids 8,11,14-eicosatrienoic acid, 5,8,11,14-eicosatetraenoic acid, and 7,10,13,16-docosatetraenoic acid generated significant amounts of MDA in a time-dependent manner when they were added to cultures of medial cells and fibroblasts [26].
• Its precursors, gamma-linolenic acid and dihomo-gamma-linolenic acid, are physiologically provided in colostrum and mature breast milk of healthy mothers [19].
• The only n-6 fatty acid showing a significant (p less than 0.05) dose-related increase was dihomo-gamma-linolenic acid (20:3n-6) in neutrophil phospholipids [27].
• Lapine articular chondrocytes were subcultured in the presence or absence of the prostanoid precursors, arachidonic acid or dihomo-gamma-linolenic acid, and the cyclooxygenase inhibitor indomethacin [28].
• Multiple linear regression analyses showed that BDI was negatively associated with eicosapentaenoic acid (EPA), while CES-D was positively associated with DGLA in adipose tissue [29].

Gene context of Dihomo-gamma-linolenic acid

• DGLA suppresses T cell activation and production of interleukin-2 (IL-2) [30].
• Evidence that suppression of IL-1 induced collagenase mRNA expression by dihomo-gamma-linolenic acid (DGLA) involves inhibition of NF kappa B binding [31].
• Administration of gamma-linolenic acid, which is converted rapidly to dihomo-gamma-linolenic acid (DGLA), reduces joint swelling and tenderness in patients with rheumatoid arthritis [30].
• In contrast, increase in the concentrations of DGLA, AA, EPA, and DHA is much less with specific COX-2 inhibitors since they do not block the formation of eicosanoids through COX-1 pathway [32].
• In addition, borage oil-, primrose oil- and fish-borage oil mixture-fed mice had significantly (P less than 0.05) higher levels of dihomo-gamma-linolenic acid [20:3(n-6)] in membrane phospholipids (5.5, 3.5 and 5.7 mol/100 mol, respectively) relative to corn oil-fed mice (2.0 mol/100 mol).(ABSTRACT TRUNCATED AT 250 WORDS)[33]

Analytical, diagnostic and therapeutic context of Dihomo-gamma-linolenic acid

• Plasma cholesteryl ester proportions of dihomo-gamma-linolenic acid (20:3 n-6) were correlated significantly with insulin sensitivity index (r=-0.319, P=0.005), fasting serum insulin levels (r=0.230, P=0.038), body mass index (r=0.242, P=0.03) and per cent body fat (r=0.329, P=0.003) in perimenopausal women (n=81) [34].
• Changes in the fatty acid composition of immune cells and plasma by intravenous injection of dihomo-gamma-linolenic acid in mice [35].
• After perfusion, dihomo-gamma-linolenic acid (mg/g) was lower in heart phospholipids from the low copper group [36].
• The formation of dihomo-gamma-linolenic acid and of arachidonic acid decreased significantly from 12% to 5% (as % of incorporated linoleic acid) between 3 and 30 serial passages whereas the linoleic acid content increased in the cells from 68% to 83% [37].
• Clinical trials of PGE1 and of the PGE1 precursors, gamma-linolenic acid (GLA) and dihomo-gamma-linolenic acid (DGLA) have shown modest therapeutic effects [38].

References