NEFA

Free fatty acids—also called unesterified (UFA) or non-esterified (NEFA) fatty acids—are fatty acids that are in the unesterified state. In plasma, longer-chain FFA are combined with albumin, and in the cell they are attached to a fatty acid-binding protein, so that in fact they are never really free. Shorter-chain fatty acids are... 

Several antidepressants, including most of the SSRIs, nefa-zodone, and duloxetine, are known to inhibit various cytochrome P-450 isoenzymes, thereby elevating plasma levels of substrates for those isoenzymes and thus potentially leading to increased adverse effects or toxicity of those drugs. The propensity to cause these drug interactions will vary with the particular antidepressant and the precise isoenzyme9,19,30 (Table 35-6). 

The clinician should bear in mind the toxic potential for the various antidepressant medications when patients already have or develop suicidality. The TCAs and MAOIs have narrow therapeutic indices, whereas the SSRIs, SNRIs, nefa-zodone, and mirtazapine have wide therapeutic indices.22... 

Buspirone generally is well tolerated and does not cause sedation. Most common side effects include dizziness, nausea, and headaches. Drugs that inhibit CYP3A4 (e.g., verapamil, diltiazem, itraconazole, fluvoxamine, nefa-zodone, and erythromycin) can increase buspirone levels. Likewise, enzyme inducers such as rifampin can reduce buspirone levels significantly. Bupirone may increase blood pressure when coadministered with an monoamine oxidase inhibitor (MAOI). 

A large open-label flexible dose study (Sanchez-Lacay etal, 2001) utilizing nefa-zodone in the treatment of major depression in a predominantly monolingual, Hispanic Caribbean population (Dominican Republic, Puerto Rico, and Cuba) revealed similar response rates and an endpoint mean dosage when compared to previous nefazodone trials with non-Hispanic patients. No serious adverse events were reported, but 42% of the subjects did not complete the study for various reasons including side effects, family, or work responsibilities. 

Plasma non-esterified fatty acids (NEFA) were elevated by infusion of a lipid emulsion and heparin with a constant rate of 1.5 ml/min (lipid emulsion, protocols [1] and [3]) and 0.4 lU/kg per minute (heparin). In protocol [2] a solution of 0.9% saline was infused as a control for the lipid emulsion. 

The lipid infusion protocol represents an experimental situation with supraphysiologically high NEFA blood levels. In the following study it was examined, whether an extrapolation of the results to physiological situations is possible. For this purpose, the effects of short term dietary interventions on IMCL levels and insulin sensitivity were studied. Twelve healthy, lean male subjects with intermediate insulin sensitivity (BMI 23.2 0.6 kg/m, GIR = 46.1+2.8 pmol/kg/min received a high caloric (HC) and a normal caloric (NC) diet. The diets had a duration of 3 days and were characterized as follows ... 

DCB, see 1,4-Dichlorobenzene o-DCB, see 1,2-Dichlorobenzene ort/to-Dichlorobenzene, see 1,2-Dichlorobenzene /n-DCB, see 1,3-Dichlorobenzene /nefa-Dichlorobenzene, see 1,3-Dichlorobenzene p-DCB, see 1,4-Dichlorobenzene para-Dichlorobenzene, see 1,4-Dichlorobenzene DCDMH, see l,3-Dichloro-5,5-dimethylhydantoin... 

Narcotic Educational Foundation of America (NEFA), 28245 Avenue Crocker, Suite 230, Santa Clarita, CA, USA, 91355-1201, (661) 775-6968, mail add.org, . 

Hedges DW, Reimherr FW, Strong RE, Halls CH, Rust C (1996) An open trial of nefa-zodone in adult patients with generalized anxiety disorder. Psychopharmacol Bull 32 671-676... 

HR Series NEFA-HR(2) kit (Wako Chemicals GmbH, 994-75409), which include the following ... 

Circulating glucose and insulin levels are the key values for a diagnosis of type II diabetes. Obesity and elevated levels of non-esterified fatty acids (NEFA) are known to cause insulin resistance and diabetes. Comorbidity of T2DM and dyslipidemia are common in animal models and in clinical populations and therefore, cholesterol, triglycerides, inflammation markers, and blood pressure are often measured within the same experiments. However, for the purpose of this chapter, we will cover only values directly linked to T2DM. 

Free fatty acids are elevated in the plasma of obese patients and are known to cause muscle and liver insulin resistance. The Wako HR series NEFA-HR(2) is an in vitro enzymatic colorimetric method assay for the quantitative determination of non-esterified fatty acids (NEFA) in serum. Perform the assay on serum collected from mice fasted for a period greater than 4 h, but less than 16 h. Perform the test on samples immediately after collection, without freezing. Also note that hemolysis in the serum samples may interfere with the assay. 

Three vesamicol derivatives FMV 56, FAA 57 and NEFA 58, have been labelled79 with NCA [18F]F" in 25%, 5% and 30% HPLC yields, respectively, and the kinetics of their brain distribution in rats and their regional distribution in monkeys studied79. The tosylate precursors have been synthesized from the corresponding alcohols with the K222/K+ complex of [18F]F in DMSO at 130°C during 10 min. 

NEFA Non-esterified Fatty Acids (also called free fatty acids, FFA)... 

GH administered to hypophysectomized rats in vivo causes a drop in the level of plasma non-esterified fatty acids (NEFA), followed by a prolonged increase in this level [89]. This appears to be due to increased utilization of lipids - increased uptake of NEFA by muscle preceding increased output by adipose tissue. As a consequence GH diverts the energy metabolism of the organism from carbohydrate utilization to lipid utilization, and acts to oppose the effects of insulin. Actions of GH on lipid metabolism are particularly marked in man, where GH levels become elevated on fasting and presumably serve to help stimulate the increased lipid utilization seen in this condition. In contrast, in the rat, GH levels fall on fasting. 

Hawley C, Sivakumaran T, Ochocki M, Ratnam S, Huber T. A preliminary safety study of combined therapy with nefa-zodone and lithium. Int J Neuropsychopharmacol 1999 2(Suppl 1) S30-1. 

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