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BACKGROUND: Worldwide, populations are ageing with significant impact on health patterns. Studies have shown that low protein, high carbohydrate diets are associated with more favourable outcomes. Plant-based diets have also been shown to have a positive impact on cardiometabolic health, weight loss and prevention of all causes of mortality.OBJECTIVE: The aim of the current study is to assess the main and interactive effects of two macronutrient interventions in a 2×2 factorial dietary design to determine their effects on appetite and health outcomes in older individuals.METHODS: Individuals aged 65 to 75 with a BMI between 20 and 35?kg/m2were recruited. Participants were provided with ad libitum access to one of four diets for four weeks, designed as a 2×2 factorial. Each dietary treatment provided 14% of energy as protein, which was either omnivorous or semi-vegetarian in origin. The remaining complement of macronutrient energy (80–82%) was either relatively high in fat (37–41% of energy) and low in carbohydrates (41–43%), or vice versa (28–29% fat with 53% carbohydrate). Study diets were provided via a meal delivery company. Self-completed questionnaires, biospecimen and clinical assessments were collected before and after intervention to assess cardio-metabolic, oral and gut health, body composition and physical performance.RESULTS: Trial status is currently ongoing (sample and data analyses).CONCLUSIONS: This study will help determine whether protein-source (plant vs animal) and fat to carbohydrate ratio have an impact on predictors of healthy ageing. These findings will also create a sound foundation on which to base nutritional interventions in older individuals to support healthy ageing.

Epidemiological studies suggest a link between fetal/early infant nutrition and adult coronary artery disease. In the present study, we examined the effects of altering nutrition during gestation, lactation and juvenile life on aortic structure and function in rats. Wistar rat dams were fed either a control or low-protein diet throughout pregnancy, or a low-protein diet for the final 7 days of gestation only. At 21 days post-partum, male pups were weaned on to a control, low-protein or high-fat diet. At 12 weeks, the offspring rats were killed. In 46 rats, aortic sections were mounted and stained to assess media thickness and elastin content. In a further 38 rats, aortic rings were suspended in an organ bath and vascular reactivity was tested with dose–response curves to the endothelium-dependent dilator acetylcholine and the endothelium-independent dilator sodium nitroprusside. Rats exposed to maternal protein restriction while in utero had a significantly decreased aortic wall thickness compared with control rats (P=0.005). Total elastin content of the aorta was also decreased by both maternal low-protein (P=0.02) and early postnatal low-protein (P=0.01) diets. Neither maternal nor postnatal low-protein or high-fat diets, however, resulted in any significant changes in arterial dilator function. In conclusion, fetal undernutrition in rats, induced via a maternal low-protein diet, causes a decrease in aortic wall thickness and elastin content without altering aortic dilator function. These changes in vascular structure may amplify aging-related changes to the vasculature and contribute to the pathophysiology of the putative link between impaired fetal growth and adult cardiovascular disease.

This study aimed to determine whether maternal protein restriction alters hepatic glycogen metabolism. Mated female rats were fed diets containing 20% protein throughout pregnancy and lactation (CONT), 8% protein throughout pregnancy and lactation (LP), or 8% protein during the last week of pregnancy only and lactation (LLP). Weights and lengths were reduced in the LLP and LP offspring compared with the CONT offspring. The LLP and LP offspring demonstrated reduced insulin concentrations at both 10 and 26 d and also failed to show the increase in insulin seen with time in the CONT offspring. Serum glucose and leptin levels increased with time but were not different among the groups; however, in relation to adiposity leptin levels were greater in the LLP and LP offspring at 26 d. The LLP and LP offspring had increased hepatic glycogen at day 10 (CONT, 75.1 ± 9.8; LLP, 103.4 ± 11.0; LP, 116.0 ± 18.4 glucose residues/g tissue) and d 26 (CONT, 183.1 ± 38.9; LLP, 395.3 ± 16.8; LP, 396.6 ± 15.1 glucose residues/g tissue). Glycogen synthase expression was increased in the LLP and LP offspring at 10 d but not 26 d; glucose transporter 2 and glycogen phosphorylase expressions were not different at either time. At 26 d glycogen synthase activity was not different; however, glycogen phosphorylase a activity was reduced. The enhanced capacity to store glycogen despite reductions in insulin secretion suggests increased insulin sensitivity possibly acting with an alternative non–insulin-dependent glycogen storage mechanism.

This study aimed to determine whether maternal protein restriction alters hepatic glycogen metabolism. Mated female rats were fed diets containing 20 protein throughout pregnancy and lactation (CONT), 8 protein throughout pregnancy and lactation (LP), or 8 protein during the last week of pregnancy only and lactation (LLP). Weights and lengths were reduced in the LLP and LP offspring compared with the CONT offspring. The LLP and LP offspring demonstrated reduced insulin concentrations at both 10 and 26 d and also failed to show the increase in insulin seen with time in the CONT offspring. Serum glucose and leptin levels increased with time but were not different among the groups; however, in relation to adiposity leptin levels were greater in the LLP and LP offspring at 26 d. The LLP and LP offspring had increased hepatic glycogen at day 10 (CONT, 75.1 ± 9.8; LLP, 103.4 ± 11.0; LP, 116.0 ± 18.4 glucose residues/g tissue) and d 26 (CONT, 183.1 ± 38.9; LLP, 395.3 ± 16.8; LP, 396.6 ± 15.1 glucose residues/g tissue). Glycogen synthase expression was increased in the LLP and LP offspring at 10 d but not 26 d; glucose transporter 2 and glycogen phosphorylase expressions were not different at either time. At 26 d glycogen synthase activity was not different; however, glycogen phosphorylase aactivity was reduced. The enhanced capacity to store glycogen despite reductions in insulin secretion suggests increased insulin sensitivity possibly acting with an alternative non–insulin-dependent glycogen storage mechanism.

Objective: Intrauterine growth restriction is associated with increased prevalence of the metabolic syndrome in adult life, including increased adiposity. The aim of this study was to investigate if maternal protein energy malnutrition is associated with changes in expression of genes involved in fat partitioning in weanling rats. Research Methods and Procedures: Time‐mated mothers were placed on one of two isocaloric diets, low protein [(LP), 8% protein] or control (20% protein). All mothers remained on the diet throughout pregnancy and lactation. A third group received control for 2 weeks and was switched to LP for the last week of pregnancy and lactation [late low protein (LLP) group]. Offspring were analyzed at weaning for serum glucose, nonesterified fatty acids, triglyceride, and insulin. Expression of the genes acetyl‐coenzyme A carboxylase, fatty acid synthase, and carnitine palmitoyl transferase 1 were measured in liver, quadriceps muscle, and subcutaneous white adipose tissue using semiquantitative reverse transcription‐polymerase chain reaction. Results: LLP and LP offspring were shorter, weighed less, had reduced serum insulin and nonesterified fatty acids, and had increased serum glucose, serum triglycerides, and hepatic triglycerides. Hepatic gene expression of acetyl‐coenzyme A carboxylase and fatty acid synthase was increased 2‐fold in LLP and LP offspring (p< 0.001). These changes were not seen in muscle or subcutaneous white adipose tissue. CPT‐1gene expression was unaltered in all tissues examined. Discussion: Maternal protein energy malnutrition programs gene expression of lipogenic enzymes in the liver of weanling offspring in a manner favoring fat synthesis that may predispose these offspring to fat accumulation and insulin resistance later in life.

Objective:Obesity is a major risk factor for the development of type 2 diabetes. Tumor necrosis factor (TNF)‐α is a candidate gene for the development of both obesity and insulin resistance. We investigated whether a common polymorphism in the promoter region (−308 G/A) of the TNF‐α gene was associated with increased risk for the development of insulin resistance and cardiovascular disease in an obese Australian population. Research Methods and Procedures:Obese, non‐diabetic subjects (146 women and 34 men) were genotyped with polymerase chain reaction‐restriction fragment length polymorphism techniques, and anthropometric and biochemical measurements were analyzed. A homeostasis model assessment (HOMA) score was used to gauge the level of insulin resistance. Results:The frequencies of the Gallele and the Aallele were 0.759 and 0.241, respectively. Subjects homozygous for the Aallele had higher fasting insulin levels (226 vs. 131 pM; p< 0.001), higher HOMA scores (10.2 vs. 5.3; p< 0.001), higher systolic blood pressure (143 vs. 129 mm Hg; p= 0.02), and lower high‐density lipoprotein (HDL) cholesterol (1.13 vs. 1.25 mM; p= 0.04) than did subjects homozygous for the Gallele. Whereas an association between insulin resistance and body mass index or waist circumference was seen in all subjects, a highly significant negative correlation of HDL cholesterol to HOMA scores (r= −0.710; p< 0.001) occurred in subjects with the Aallele only. Discussion:The −308 G/ATNF‐α gene variant conveys an increased risk for the development of insulin resistance in obese subjects. The presence of low HDL cholesterol levels further increases the risks associated with insulin resistance in carriers of the Aallele.