Absorption, Distribution and Excretion
The objectives of this study were: 1) to quantify the systemic concentration of linoleic acid (LA) in the human body using the systemic fatty acid balance method; 2) to estimate the distribution of LA in adipose tissue and lean tissue; and 3) to assess the effects of weight loss on LA storage and β-oxidation in obese individuals. Nine healthy obese men underwent a 112-day (16-week) supervised weight loss program. Magnetic resonance imaging (MRI) data and fatty acid profiling from fat biopsies were used to determine LA storage in adipose tissue, lean tissue, and throughout the body. LA β-oxidation was calculated as: intake - (accumulation + excretion). During the study, the average weight loss was 13 kg, with LA intake of 24 ± 6 mmol/d. Systemic LA loss was 37 ± 18 mmol/d, equivalent to 28% of pre-weight loss levels. The sum of LA intake and systemic loss indicated that LA β-oxidation during weight loss was 2.5 times the intake. All dietary linoleic acid is β-oxidized, and obese men lose at least an equivalent amount of linoleic acid during moderate weight loss. This study's methods can assess long-term changes in linoleic acid homeostasis in obese individuals and may help determine the risk of linoleic acid deficiency in other situations. /Linoleic Acid/
The fatty acid composition of breast milk varies with the mother's dietary fat composition. Hydrogenated cooking oils containing trans fatty acids may displace or adversely affect the metabolism of cis-n-6 and n-3 unsaturated fatty acids. Although n-6 and n-3 fatty acids are essential for infant growth and development, the effects of trans fatty acids, n-6 fatty acids, and n-3 fatty acids in breast milk on breastfed infants are unclear. This study aimed to determine the relationship between trans and cis-unsaturated fatty acids in breast milk, plasma phospholipids, and triglycerides, and to identify the major sources of trans fatty acids in the maternal diet. The study collected breast milk from 103 mothers who exclusively breastfed 2-month-old infants, blood samples from 62 infants, and 3-day dietary records from 21 mothers. Results: The mean percentages (± standard errors) of trans fatty acids were as follows: breast milk, 7.1±0.32%; infant triglycerides, 6.5±0.33%; infant phospholipids, 3.7±0.16%. Trans fatty acids in breast milk, including α-linolenic acid (18:3n-3), arachidonic acid (20:4n-6), docosahexaenoic acid (22:6n-3) (P < 0.001), and linoleic acid (18:2n-6) (P = 0.007), were all correlated with the same fatty acids in infant plasma phospholipids. Trans fatty acids in breast milk were negatively correlated with 18:2n-6 and 18:3n-3 in breast milk, but not with 20:4n-6 or 22:6n-3 in breast milk or infant plasma. Trans fatty acids accounted for 7.7% of the mother's total fat intake (2.5% of total energy); the main dietary sources were baked goods and bread (32%), snacks (14%), fast food (11%), and margarine and shortening (11%). The concentrations of trans fatty acids in plasma triglycerides were comparable in the mother's diet, breast milk, and breastfed infants. Processed foods were the main dietary source of trans fatty acids. Partially conjugated linoleic acid (CLA) appears to be incorporated into phospholipids in cell membranes. Metabolism/Metabolites/Other Toxicity Information/ This study investigated the effects of oral administration of linoleic acid secondary autoxidation products on hepatotoxicity in rats and compared them with saline and linoleic acid control groups. Results showed a significant reduction in de novo fatty acid synthesis in the secondary product group. The level of nicotinic adenine dinucleotide phosphate (NADPH) in the liver was significantly reduced, while the level of nicotinic adenine dinucleotide (NADH) remained unchanged. The activities of glucose-6-phosphate dehydrogenase and phosphoglucuronide dehydrogenase were significantly reduced. In the secondary product group, the activities of NAD+ kinase and NAD+ synthase are decreased, while the activities of NAD+ nucleosidase are increased. Therefore, the depletion of nicotinic adenine dinucleotide phosphate (NDP) can be attributed to the inhibition of two metabolic systems (the NDP/NAD synthesis system) and leads to reduced hepatic lipogenesis. /Auto-oxidation products/
…Linoleic acid stimulates tumor growth because it can be converted into the mitogen 13-hydroxyoctadecadienoic acid (13-HODE) by hepatocellular carcinoma 7288CTC. …
Cyclic adenosine monophosphate (cAMP) enhances the synthesis of 13-hydroxyoctadecadienoic acid (13-HODE). Gamma-linolenic acid (GLA), a desaturated metabolite of linoleic acid, significantly stimulates the synthesis of 13-hydroxydecanoic acid glyceride (13-HODE). The decline in GLA synthesis with age may be related to the age-related decline in 13-HODE production. /γ-Linolenic acid/
Linoleic acid's known metabolites include leukotoxin and isoleukotoxin.

Linoleic acid is a colorless to pale yellow liquid and an essential polyunsaturated fatty acid for the human body. Linoleic acid is an octadecadienoic acid with two double bonds located at positions 9 and 12, exhibiting a Z (cis) stereochemical configuration. It is found in plants, water fleas (Daphnia galeata), and algae as a metabolite. It is an omega-6 fatty acid, also an octadecadienoic acid, and the conjugate acid of linoleic acid. Linoleic acid has been reported to be found in Calodendrum capense, tea trees (Camellia sinensis), and other organisms with relevant data. Linoleic acid is a polyunsaturated essential fatty acid, primarily found in vegetable oils. It participates in the biosynthesis of prostaglandins and cell membranes. Linoleic acid is a diunsaturated fatty acid, also known as an omega-6 fatty acid, widely found in plant glycosides. In this particular polyunsaturated fatty acid (PUFA), the first double bond is located between the sixth and seventh carbon atoms at the (n-6) methyl terminus of the fatty acid. Linoleic acid is an essential fatty acid in human nutrition because it cannot be synthesized by the human body. It participates in the biosynthesis of prostaglandins (via arachidonic acid) and cell membranes. (From Stedman, 26th edition)
A diunsaturated fatty acid, widely found in plant glycosides. It is an essential fatty acid in mammalian nutrition and participates in the biosynthesis of prostaglandins and cell membranes. (From Stedman, 26th edition)
See also: cod liver oil (partial); krill oil (partial); saw palmetto (partial)...see more...

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Mechanism of Action
/The purpose of this study is/to investigate the expression of the resistin gene in white adipose tissue and its interaction with conjugated linoleic acid during the formation of insulin resistance in obese rats fed a high-fat diet. Male Wistar rats were randomly divided into a control group, a high-fat group, and a high-fat + conjugated linoleic acid (CLA) group (0.75 g, 1.50 g, and 3.00 g CLA were added per 100 g of diet, respectively). The expression levels of resistin and peroxisome proliferation activation receptor γ (PPARγ) mRNA were detected by reverse transcription polymerase chain reaction (RT-PCR). The serum insulin and glucose levels of obese rats were (11.11±2.73) mIU/L and (5.09±0.66) mmol/L, respectively. CLA supplementation may reduce hyperinsulinemia and hyperglycemia. In the CLA groups (0.75 g, 1.50 g, and 3.00 g per 100 g feed weight), serum insulin levels were (6.99±1.77) mIU/L, (7.36±1.48) mIU/L, and (7.85±1.60) mIU/L, respectively, and glucose levels were (4.28±0.72) mmol/L, (4.18±0.55) mmol/L, and (4.06±0.63) mmol/L, respectively. Compared with obese rats fed a basal diet, obese rats fed a high-fat diet showed increased resistin expression in adipose tissue. Conjugated linoleic acid (CLA) may increase the expression of resistin and peroxisome proliferator-activated receptor γ (PPARγ) in the adipose tissue of obese rats. The resistin mRNA expression in obese rats fed a high-fat diet was higher than that in obese rats fed a basal diet. CLA may improve insulin resistance in obese rats and may upregulate resistin expression by activating PPARγ. Conjugated linoleic acid (CLA) is a mixture of positional isomers (e.g., 7,9; 9,11; 10,12; 11,13) and geometric isomers (cis or trans). This compound was initially shown to prevent mammary cancer in mice. Subsequent studies have revealed numerous other health benefits, including reduced atherosclerosis and inflammation, while enhancing immune function. The mechanisms underlying these biological properties are not fully understood. This review aims to highlight recent advances in the study of CLA in experimental inflammatory bowel disease. Furthermore, two possible mechanisms of action of CLA in inflammatory bowel diseases (i.e., endoplasmic reticulum and nuclear) are discussed in detail. CLA was initially thought to downregulate the production of inducible eicosate derivatives (such as PGE₂ and LTB₄) involved in early microinflammatory events (endoplasmic reticulum). Recent studies have shown that CLA can modulate gene expression regulated by peroxisome proliferator-activated receptors (PPARs; nuclear). In a pig model, long-term dietary CLA supplementation stimulated PPAR-γ expression in muscle. Therefore, existing evidence supports the two-mechanism theory that CLA exerts its effects through eicosate synthesis and PPAR activity. Further understanding of the anti-inflammatory mechanism of CLA holds promise for providing new nutritional therapies for the treatment of intestinal inflammation. Conjugated linoleic acid (CLA) may regulate arachidic acid activity and tumor necrosis factor-α activity.

C18H32O2

280.4455

280.24

60-33-3

7049-66-3;30175-49-6;67922-65-0

5280450

Colorless oil
Colorless to straw-colored liquid

0.9±0.1 g/cm3

360.6±0.0 °C at 760 mmHg

-5 °C

273.0±14.4 °C

0.0±1.7 mmHg at 25°C

1.478

7.18

1

2

14

20

267

0

O([H])C(C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])/C(/[H])=C(/[H])\C([H])([H])/C(/[H])=C(/[H])\C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H])=O

OYHQOLUKZRVURQ-HZJYTTRNSA-N

InChI=1S/C18H32O2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18(19)20/h6-7,9-10H,2-5,8,11-17H2,1H3,(H,19,20)/b7-6-,10-9-

(9Z,12Z)-octadeca-9,12-dienoic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)