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Diabetes Care 30:e55 2007
DOI: 10.2337/dc07-0361
© 2007 by the American Diabetes Association
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Online Letters: Comments and Responses

Prevalence of Nonalcoholic Fatty Liver Disease and Its Association With Cardiovascular Disease Among Type 2 Diabetic Patients

Response to Targher et al. and Hu et al.

Manisha Talim, MBBS, DD

From Shushrusha Hospital, Mumbai, India

Address correspondence to Dr. Manisha Talim, Shushrusha Hospital, 698B Ranade Rd., Dadar, Mumbai 400028, India. E-mail: drmanishatalim{at}yahoo.com

I read with interest the articles by Targher et al. (1), which shows that nonalcoholic fatty liver disease (NAFLD) is extremely common in type 2 diabetes and is associated with a higher prevalence of cardiovascular disease (CVD), and by Hu et al. (2), which shows that type 2 diabetes is associated with an increased risk of Parkinson's disease. Neither is surprising, considering society's excessive use of polyunsaturated n-6–rich vegetable oils (a source of linoleic acid, a short-chain n-6 polyunsaturated fatty acid [PUFA]) in place of saturated fats, in addition to a deficiency of n-3 fat. It is possible to hypothesize that Parkinson's disease, CVD, and diabetes share common ground linked by improper diet.

Svegliati-Baroni et al. (3) have demonstrated that supplementation of n-3 PUFA ameliorates fatty liver and degree of liver injury in rats. In humans, a high-fat intake, particularly of n-6 fat and a high n-6:n-3 ratio, was found in patients of nonalcoholic steatohepatitis (4).

A diabetes prevention study in Eskimos demonstrated that a higher consumption of long-chain n-3 fatty acids was associated with improved glucose tolerance, insulin resistance, and components of the metabolic syndrome (5).

Diabetes, heart disease, and NAFLD appear to be chronic inflammatory conditions in response to inadequate or improper diet. As demonstrated by Julien et al. (6), nutritional intake affects brain fatty acids and is a determinant of Parkinson's disease. The same applies to diabetes (7), and the benefit of n-3 fat in CVD is also well known. Long-chain n-3 PUFAs decrease triglycerides, inflammatory eicosanoids and cytokines, blood pressure, and thrombosis and increase nitric oxide production and endothelial relaxation (8).

A problem in Parkinson's disease is the decrease in dopamine. Studies also show that Parkinson's patients who experienced motor complications due to levodopa had higher arachidonic acid concentrations in the cortex compared with control subjects and levodopa-treated patients devoid of motor complications (6).

PUFAs are required in the ratio of n6:n3 of <5:1. Arachidonic acid and docosahexanoic acid are longer PUFAs of n-6 and n-3, respectively. In proper proportion, their intake determines homeostasis of various body tissues including nervous tissue. Animal studies reveal that n-3 fatty acid deficiency decreases dopamine receptor binding (9) and alters dopamine metabolism (10), and supplementation with long-chain PUFAs prevents the decrease in dopaminergic neurotransmitters in the frontal cortex caused by deficiency in alphalinolenic acid (n-3 fat) (11).

Universal recommendations to correct PUFA imbalance are needed to prevent diabetes and a host of diseases including Parkinson's disease, heart disease, and NAFLD. Implications point to a solution for preventing all the four diseases: correction of inadequate or improper diet; therefore there is an urgent need for large-scale studies in this respect.

References

  1. Targher G, Bertolini L, Padovani R, Rodella S, Tessari R, Zenari L, Christopher D, Arcaro G: Prevalence of nonalcoholic fatty liver disease and its association with cardiovascular disease among type 2 diabetic patients. Diabetes Care 30:1212–1218, 2007[Abstract/Free Full Text]
  2. Hu G, Jousilahti P, Bidel S, Antikainen R, Tuomilehto J: Type 2 diabetes and the risk of Parkinson's disease. Diabetes Care 30:842–847, 2007[Abstract/Free Full Text]
  3. Svegliati-Baroni G, Candelaresi C, Saccomnno S, Ferretti G, Bachetti T, Marzioni M, De Minicis S, Nobili L, Salzano R, Omenetti A, Pacetti D, Sigmund S, Benedetti A, Casini A: A model of insulin resistance and nonalcoholic steatohepatitis in rats: role of peroxisome proliferators-activated receptor alpha and n-3 polyunsaturated fatty acid treatment on liver injury. Am J Pathol 169:846–860, 2006[Abstract/Free Full Text]
  4. Cortez-Pinto H, Jesus L, Barros H, Lopes C, Moura M, Camilo M: How different is the dietary pattern in non-alcoholic steatohepatitis patients? Clin Nutr 25:816–823, 2006[Medline]
  5. Ebbeson S, Ebbesson L, Swenson M, Kennish J, Robbins DA: Successful diabetes prevention study in Eskimos: the Alaska Siberia Project. Int J Circumpolar Health 64:409–424, 2005[Medline]
  6. Julien C, Berthiaume L, Hadj-Tahar A, Rajput A, Bedard P, Di Paolo T, Julien P, Calon F: Postmortem brain fatty acid profile of levodopa-treated Parkinson disease patients and parkinsonian monkeys. Neurochem Int 48:404–414, 2006[Medline]
  7. Raheja B, Talim M: Dietary fats and their lipid toxicity: role in pathogenesis of CHD, diabetes and cancer. J Diab Assoc India 38:1–11, 1998
  8. Calder P: n-3 Fatty acids and cardiovascular disease: evidence explained and mechanisms explored. Clin Sci (Lond) 107:1–11, 2004[Medline]
  9. Delion S, Chalon S, Herault J, Gulloteau D, Besnaud J, Durand G: Chronic alpha-linolenic acid deficiency alters dopaminergic and serotonergic neurotransmission in rats. J Nutr 124:2466–2476, 1994[Abstract/Free Full Text]
  10. De la Presa O, Innis S: Docosahexanoic and arachidonic acid prevent a decrease in dopaminergic and serotoninergic neurotransmitters in frontal cortex caused by linoleic and alphalinolenic acid deficient diet in formula fed piglets. J Nutr 129:2088–2093, 1999[Abstract/Free Full Text]
  11. Zimmer I, Hembert S, Dward G, Breton P, Guilloteau D, Besnard J-C, Chalon S: Chronic n-3 polyunsaturated fatty acid deficiency acts on dopamine metabolism in the rat frontal cortex: a microdialysis study. Neurosci Lett 240:177–181, 1998[Medline]

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G. Hu, P. Jousilahti, and J. Tuomilehto
Prevalence of Nonalcoholic Fatty Liver Disease and Its Association With Cardiovascular Disease Among Type 2 Diabetic Patients: Response to Talim
Diabetes Care, June 1, 2007; 30(6): e56 - e56.
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