linoleic-acid and Diabetic-Neuropathies

Linoleic acid is the main dietary essential fatty acid (EFA). To be fully utilized by the body, it must be metabolized to a range of other substances. The first step in this pathway is delta-6-desaturation to gamma-linolenic acid (GLA). This step is slow and rate-limiting, particularly in humans. If delta-6-desaturation is impaired for any reason, the supply of further metabolites may be inadequate for normal function. If the consumption of further metabolites is excessive, then a normal rate of delta-6-desaturation may be inadequate. In these circumstances the direct supply of GLA or further metabolites may be of value. This concept is illustrated by atopic eczema and diabetes, which may represent inherited and acquired examples of inadequate delta-6-desaturation.

Topics: Dermatitis, Atopic; Diabetes Mellitus; Diabetic Neuropathies; Fatty Acid Desaturases; Fatty Acids, Essential; gamma-Linolenic Acid; Humans; Linoleic Acid; Linoleic Acids; Linolenic Acids; Linoleoyl-CoA Desaturase

This study investigated the association between dietary intake of polyunsaturated fatty acids (PUFAs) and peripheral neuropathy in the U.S. population.. We analyzed data from the National Health and Nutrition Examination Survey (NHANES) 1999-2004 for adults >or=40 years of age with diagnosed diabetes, an assessment of peripheral neuropathy, and reliable 24-h dietary recall. The dietary intake of PUFAs was analyzed by peripheral neuropathy status. Multivariate logistic regression models were used to estimate the odds of having peripheral neuropathy in higher quintiles of PUFA intake compared with the lowest quintile.. The mean dietary intake of linolenic acid was 1.25 +/- 0.07 g among adults with peripheral neuropathy, significantly lower than the 1.45 +/- 0.05 g intake among those without peripheral neuropathy. After controlling for potential confounding variables, adults whose linolenic acid intake was in the highest quintile had lower odds of peripheral neuropathy than adults in the lowest quintile (adjusted odds ratio 0.40 [95% CI 0.21-0.77]).. Among adults with diagnosed diabetes, dietary intake of linolenic acid is positively associated with lower odds of peripheral neuropathy.

Topics: Adult; Diabetes Mellitus; Diabetic Neuropathies; Dietary Fats; Fatty Acids, Unsaturated; Health Surveys; Humans; Linoleic Acid; Multivariate Analysis; Nutritional Status; Peripheral Nervous System Diseases; United States

Peripheral nerve involvement is a frequent complication of type 1 and type 2 diabetes, and can induce major disability. Almost all types of clinical or electrophysiological disturbances may be present: mononeuropathy involving cranial nerves or a limb; multiple mononeuropathy; proximal acute radiculopathy; distal, symmetric, sensory polyneuropathy; autonomic neuropathy. Physiopathology intricates probably several mechanisms but metabolic dysregulation and ischemia are mainly involved. Despite numerous controlled clinical trials no treatment has demonstrated efficacy for peripheral neuropathy, excepting the optimization of diabetes equilibrium. However, symptomatic treatments are available, particularly for the management of neuropathic pain.

Topics: Acetates; Amines; Animals; Anti-Inflammatory Agents, Non-Steroidal; Carbamazepine; Controlled Clinical Trials as Topic; Cyclohexanecarboxylic Acids; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetic Neuropathies; Double-Blind Method; Electrophysiology; Gabapentin; gamma-Aminobutyric Acid; Humans; Hyperglycemia; Immunoglobulins, Intravenous; Linoleic Acid; Pain; Prognosis

Topics: Diabetic Neuropathies; Drug Contamination; gamma-Linolenic Acid; Humans; Linoleic Acid; Linoleic Acids

Early effects of insulin and essential fatty acids on nerve conduction were studied. Insulin-dependent diabetes was induced in rats using streptozocin (65 mg/kg, i.p.); control rats were treated with buffer. Five weeks later, diabetic rats were divided into 5 groups. Two groups were given oral essential fatty acids (75% linoleic and 9% gamma-linolenic acids) for a further 3 and 5 days, respectively. Two other groups received subcutaneous insulin for a further 3 or 5 days. A group of diabetic rats were left without further treatment. Motor nerve conduction velocity was measured terminally in all rats by stimulating the sciatic nerve and recording EMGs in the gastrocnemius muscle under urethane anaesthesia. Sensory nerve conduction velocity was measured by stimulating and recording from the saphenous nerve trunk. Diabetic rats had significantly slowed motor and sensory nerve conduction velocities after 5 weeks (16.7%, P less than 0.001). Three days treatment with either insulin or fatty acids corrected the slowed motor nerve conduction velocity to a normal level. Conduction velocity in myelinated sensory nerves was still 10% slower in diabetic rats treated with insulin for 3 days (P less than 0.01). It was above the control level by 11% in diabetic rats treated with fatty acids for the same period (P less than 0.01). Conduction velocities in both sensory and motor nerves were normal in diabetic rats treated with either insulin or fatty acids for 5 days. It was concluded that both insulin and essential fatty acids had early effects on nerve conduction in diabetic rats. The speed of their actions, and the magnitudes of responses were different in sensory and motor nerves.

Topics: Animals; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Female; gamma-Linolenic Acid; Insulin; Linoleic Acid; Linoleic Acids; Linolenic Acids; Motor Neurons; Neural Conduction; Neurons, Afferent; Rats; Rats, Inbred Strains; Streptozocin