X-Message-Number: 24585
Date: Thu, 2 Sep 2004 20:31:14 -0700 (PDT)
From: Doug Skrecky <>
Subject: dietary prevention of nephropathy

[For such a simple intervention the longevity results were surprisingly
robust. Maximum lifespan of "short-lived" NOD mice was 11 months on
standard AIN-93G chow. By contrast 78% of NOD mice fed the low AGE diet
were alive at 14 months, which was the end of the study. What was this
wonderful low AGE diet? It was also AIN-93G chow, which however was
deprived of its "normal" 125 C X 20-30 minute heat treatment. I am amazed
at the longevity decrease simple heat treatment of chow can cause! I'm
wondering what its effect on "normal" long-lived mice would be.]

Diabetes Metab Res Rev. 2002 May-Jun;18(3):224-37.
Prevention of diabetic nephropathy in mice by a diet low in glycoxidation
products.
  BACKGROUND: Reactive advanced glycation end products (AGEs), known to
promote diabetic tissue damage, occur endogenously as well as in heated
foods and are orally absorbed. The relative contribution of diet-derived
AGEs to diabetic nephropathy (DN) remains unclear. METHODS: We tested a
standard mouse food (AIN-93G) found to be rich in AGEs (H-AGE diet) in
parallel with a similar diet that contained six-fold lower AGE content
(L-AGE), but equal calories, macronutrients, and micronutrients.
Non-obese diabetic mice (NOD) with type 1 diabetes (T1D) and db/db mice
with type 2 diabetes (T2D) were randomly assigned to each formula for
either 4 or 11 months, during which time renal parameters and AGE levels
were assessed. RESULTS: Compared to the progressive DN and short survival
seen in NOD mice exposed to long-term H-AGE feeding, L-AGE-fed NOD mice
developed minimal glomerular pathology and a modest increase in urinary
albumin:creatinine ratio (p<0.005), and a significantly extended survival
(p<0.0001), consistent with lower serum (p<0.025) and kidney AGEs
(p<0.01). Also, in the 4-month study, and in contrast to the H-AGE-fed
mice, L-AGE-fed NOD and db/db mice exhibited low levels of renal cortex
TGF beta-1 (p<0.05), laminin B1 mRNA (p<0.01) and alpha 1 IV collagen
mRNA (p<0.05) and protein, in concert with reduced serum and kidney AGEs
(p<0.05, respectively). CONCLUSION: Intake of high-level, food-derived
AGEs is a major contributor to DN in T1D and T2D mice. Avoidance of
dietary AGEs provides sustained protection against DN in mice; providing
the rationale for similar studies in human diabetic patients.

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