Abstract
Because chronic hyperglycemia of uncontrolled diabetes mellitus may lead to increased reactive oxygen species and decreased enzymatic antioxidant defenses responsible for pathological processes in diabetic retinopathy, this study examined the hypothesis that a low-carbohydrate, high-fat diet, either alone or in combination with Pinus maritima can reduce hyperglycemia, restoring a more balanced, oxidative condition. Normal and streptozotocin-induced diabetic rats were fed either a regular or low-carbohydrate diet for 30 or 90 d. In addition, normal and diabetic rats on the chronic (90-d) low-carbohydrate diet were treated with daily intraperitoneal Pinus maritima doses (10 mg/kg) for 14 consecutive days. Retinas were fractionated to assay activities of glutathione peroxidase, glutathione reductase, and γ-glutamyl transferase. After 30 d, the low-carbohydrate diet reduced glycemic parameters and normalized aspartate aminotransferase activity in diabetic animals, suggesting less organ damage. No differences were observed between males and females in any measured glycemic parameters. Whereas all diabetic control animals developed cataracts bilaterally, no treated diabetic animals developed cataracts. There were no deleterious effects on retinal antioxidant defenses with either a 30-d or chronic low-carbohydrate diet. When diet was combined with Pinus maritima treatment, both retinal glutathione peroxidase and glutathione reductase activities increased, suggesting that a low-carbohydrate diet plus Pinus maritima may be an effective antioxidant and antihyperglycemic therapy, reducing the risk of diabetic retinopathy and cataract formation.
| Original language | English |
|---|---|
| Pages (from-to) | 10-18 |
| Number of pages | 9 |
| Journal | Journal of Ocular Pharmacology and Therapeutics |
| Volume | 22 |
| Issue number | 1 |
| DOIs | |
| State | Published - Feb 2006 |
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ASJC Scopus subject areas
- Pharmacology (medical)
- Ophthalmology
- Pharmacology, Toxicology and Pharmaceutics(all)
Cite this
Effects of low-carbohydrate diet and Pycnogenol® treatment on retinal antioxidant enzymes in normal and diabetic rats. / Kamuren, Zipporah T.; McPeek, Chris G.; Sanders, Ruth A.; Watkins, John B.
In: Journal of Ocular Pharmacology and Therapeutics, Vol. 22, No. 1, 02.2006, p. 10-18.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of low-carbohydrate diet and Pycnogenol® treatment on retinal antioxidant enzymes in normal and diabetic rats
AU - Kamuren, Zipporah T.
AU - McPeek, Chris G.
AU - Sanders, Ruth A.
AU - Watkins, John B.
PY - 2006/2
Y1 - 2006/2
N2 - Because chronic hyperglycemia of uncontrolled diabetes mellitus may lead to increased reactive oxygen species and decreased enzymatic antioxidant defenses responsible for pathological processes in diabetic retinopathy, this study examined the hypothesis that a low-carbohydrate, high-fat diet, either alone or in combination with Pinus maritima can reduce hyperglycemia, restoring a more balanced, oxidative condition. Normal and streptozotocin-induced diabetic rats were fed either a regular or low-carbohydrate diet for 30 or 90 d. In addition, normal and diabetic rats on the chronic (90-d) low-carbohydrate diet were treated with daily intraperitoneal Pinus maritima doses (10 mg/kg) for 14 consecutive days. Retinas were fractionated to assay activities of glutathione peroxidase, glutathione reductase, and γ-glutamyl transferase. After 30 d, the low-carbohydrate diet reduced glycemic parameters and normalized aspartate aminotransferase activity in diabetic animals, suggesting less organ damage. No differences were observed between males and females in any measured glycemic parameters. Whereas all diabetic control animals developed cataracts bilaterally, no treated diabetic animals developed cataracts. There were no deleterious effects on retinal antioxidant defenses with either a 30-d or chronic low-carbohydrate diet. When diet was combined with Pinus maritima treatment, both retinal glutathione peroxidase and glutathione reductase activities increased, suggesting that a low-carbohydrate diet plus Pinus maritima may be an effective antioxidant and antihyperglycemic therapy, reducing the risk of diabetic retinopathy and cataract formation.
AB - Because chronic hyperglycemia of uncontrolled diabetes mellitus may lead to increased reactive oxygen species and decreased enzymatic antioxidant defenses responsible for pathological processes in diabetic retinopathy, this study examined the hypothesis that a low-carbohydrate, high-fat diet, either alone or in combination with Pinus maritima can reduce hyperglycemia, restoring a more balanced, oxidative condition. Normal and streptozotocin-induced diabetic rats were fed either a regular or low-carbohydrate diet for 30 or 90 d. In addition, normal and diabetic rats on the chronic (90-d) low-carbohydrate diet were treated with daily intraperitoneal Pinus maritima doses (10 mg/kg) for 14 consecutive days. Retinas were fractionated to assay activities of glutathione peroxidase, glutathione reductase, and γ-glutamyl transferase. After 30 d, the low-carbohydrate diet reduced glycemic parameters and normalized aspartate aminotransferase activity in diabetic animals, suggesting less organ damage. No differences were observed between males and females in any measured glycemic parameters. Whereas all diabetic control animals developed cataracts bilaterally, no treated diabetic animals developed cataracts. There were no deleterious effects on retinal antioxidant defenses with either a 30-d or chronic low-carbohydrate diet. When diet was combined with Pinus maritima treatment, both retinal glutathione peroxidase and glutathione reductase activities increased, suggesting that a low-carbohydrate diet plus Pinus maritima may be an effective antioxidant and antihyperglycemic therapy, reducing the risk of diabetic retinopathy and cataract formation.
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U2 - 10.1089/jop.2006.22.10
DO - 10.1089/jop.2006.22.10
M3 - Article
VL - 22
SP - 10
EP - 18
JO - Journal of Ocular Pharmacology and Therapeutics
JF - Journal of Ocular Pharmacology and Therapeutics
SN - 1080-7683
IS - 1
ER -