Six healthy male volunteers underwent 2-wk metabolically controlled high-glycemic-index (GI) and low-GI diets in random order. Over the low-GI diet significant reductions were seen in serum fructosamine (7.0 +/- 1.0%, p less than 0.01), 12-h blood glucose profile (37 +/- 7%, p less than 0.01), and total serum cholesterol (15 +/- 3%, p less than 0.01). As a measure of insulin secretion, 24-h urinary C-peptide levels were 32 +/- 10% lower (p less than 0.05) after the low-GI than after the high-GI diet. Lower C-peptide levels were maintained after a standard carbohydrate challenge after the low-GI diet despite higher blood glucose levels. Differences in blood glucose were not seen after a 5-g intravenous glucose challenge. These results are of interest with respect to the effect that prolonged postprandial reductions in nutrient fluxes and insulin secretion may have on carbohydrate and lipid metabolism and renal function.

Mammalian lignan production from flaxseed precursors is dependent on time and dose but not on processing.

No abstract

Glycyrrhizic acid (GA) ameliorates many components of the metabolic syndrome, but its potential therapeutic use is marred by edema caused by inhibition of renal 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2). We assessed whether 100 mg/kg per day GA administered orally could promote metabolic benefits without causing edema in rats fed on a high-sucrose diet. Groups of eight male rats were fed on one of three diets for 28 days: normal diet, a high-sucrose diet, or a high-sucrose diet supplemented with GA. Rats were then culled and renal 11β-HSD2 activity, as well as serum sodium, potassium, angiotensin II and leptin levels were determined. Histological analyses were performed to assess changes in adipocyte size in visceral and subcutaneous depots, as well as hepatic and renal tissue morphology. This dosing paradigm of GA attenuated the increases in serum leptin levels and visceral, but not subcutaneous adipocyte size caused by the high-sucrose diet. Although GA decreased renal 11β-HSD2 activity, it did not affect serum electrolyte or angiotensin II levels, indicating no onset of edema. Furthermore, there were no apparent morphological changes in the liver or kidney, indicating no toxicity. In conclusion, it is possible to reap metabolic benefits of GA without edema using the current dosage and treatment time.