The dietary reference intakes (DRIs) established an acceptable macronutrient distribution range (AMDR); however, few studies have evaluated differences in metabolic regulations across the DRI range. This study examined differences in glycemic regulations associated with specific ratios of carbohydrate and protein. Male rats ( approximately 200 g) were fed either a high-carbohydrate diet (CHO group: 60% of energy as carbohydrates, 12% protein, 28% fat) or a reduced-carbohydrate diet [PRO (protein) group: 42% carbohydrates, 30% protein, 28% fat]. Rats consumed 3 meals/d with energy distributed as 16, 42, and 42%. On d 25, blood and tissues were obtained after 12 h of food deprivation and at 30 and 90 min after the first meal. Before the meal, the CHO group had lower plasma glucose and insulin, reduced liver glycogen, lower expression of hepatic phosphoenolpyruvate carboxylase (PEPCK), and increased fatty acid synthase (FAS) in adipose tissue. After the meal, the CHO group had greater increases in plasma glucose and insulin, producing increased skeletal muscle phosphatidylinositol 3-kinase (PI3-kinase) activity, glucose uptake, and glycogen content, and increased adipose PI3-kinase activity, glucose uptake, and FAS. In contrast, the PRO group had limited postprandial changes in plasma glucose and insulin with reduced muscle PI3-kinase activity and glucose uptake, and no postprandial changes in adipose PI3-kinase activity or FAS. This study demonstrates that changes in carbohydrate and protein intakes within the AMDR produce fundamental shifts in glycemic regulation from high-CHO diets that require insulin-mediated peripheral glucose disposal to high-PRO diets that increase hepatic regulation of glucose appearance into the blood.
Our laboratory previously reported differential metabolic regulations in rats and humans fed low or high carbohydrate diets designed to meet DRI guidelines for macronutrients. This study examined the impact of short‐term feeding of low vs. high carbohydrate diets (LC vs. HC) on gene expression of liver enzymes involved in carbohydrate metabolism and insulin signaling in skeletal muscle and adipose. LC and HC diets consisted of 42:30:28 (carbohydrate:protein:fat as % energy) and 60:12:28, respectively. Male SD rats ~250 g were fed 3 times/d to mimic human meal patterns. After 10 d, samples were obtained at fasted (n=8) or 90 min after a 4 g meal (n=8). Plasma insulin, glucagon, glucose, and triacylglyceride were not different in fasted samples. Liver gene expression of PEPCK, pyruvate kinase, glucose‐6‐phosphatase, and fatty acid synthetase was not different between diets. Insulin and triacylglyceride increased 97% (P<0.05) and 123% (P<0.10) after the HC meal, respectively, but increased only 51% (P<0.10) and 52% (P<0.10) after the LC meal. In skeletal muscle, LC caused greater activation (p=0.01) of Akt and p70S6K (p<0.05), while HC activated Akt (p<0.05) in adipose. In summary, short‐term feeding of LC and HC diets elicited no differences in hepatic gene expression of enzymes for carbohydrate metabolism, but produced differential insulin signaling in skeletal muscle and adipose.Support: Unigen Pharmaceutical
Peroxisome proliferator‐activated receptor γ (PPARγ) is a nuclear hormone receptor that plays a key role in adipocyte differentiation. PPARα belongs to the same nuclear receptor family and regulates genes involved in fatty acid oxidation. Previously, we had shown that lycopene (LYC) feeding decreased expression of PPARγ and its target gene, fatty acid binding protein 3 (FABP3), in selected rat tissues. To evaluate the effects of phytofluene (PF), LYC or tomato powder (TP) consumption and androgen status on PPARγ and PPARα expression, 8 wk old male Fisher 344 rats were castrated or sham‐operated and subsequently provided with oral supplementation of PF or LYC (~0.7 mg/d) or fed a 10% tomato powder or control diet (AIN‐93G) for 4 days. In the liver of intact rats, PF and LYC decreased expression of PPARα and its target gene CYP 4A2. PF, LYC, and TP also reduced PPARγ expression in the adipose tissue of intact rats. Carotenoid monooxygenase I (CMO I), a PPARγ target gene, followed PPARγ expression patterns in various tissues. CMO II appeared to remain constitutively active. These results suggest a possible role of phytofluene and lycopene in lipid metabolism via modulation of PPARγ and PPARα expression.
(Funded in part by NIH/NCI CA 112649‐01A1)
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