The role of postprandial thermogenesis in the development of impaired glucose tolerance and type II diabetes.

Accounting for 5%-15% of total daily energy expenditure, postprandial thermogenesis (PPT) refers to an acute increase in resting metabolic rate (RMR) in the hours after eating. This is largely explained by the energy costs of processing the macronutrients of a meal. Most individuals spend the majority of the day in the postprandial state, thus over one's lifetime even minor differences in PPT may possess true clinical significance. In contrast to RMR, research indicates that PPT may be reduced in the development of both prediabetes and type II diabetes (T2D). The present analysis of existing literature has found that this impairment may be exaggerated in hyperinsulinemic-euglycemic clamp studies compared with food and beverage consumption studies. Nonetheless, it is estimated that daily PPT following carbohydrate consumption alone is approximately 150 kJ lower among individuals with T2D. This estimate fails to consider protein intake, which is notably more thermogenic than carbohydrate intake (20%-30% vs. 5%-8%, respectively). Putatively, dysglycemic individuals may lack the insulin sensitivity required to divert glucose toward storage-a more energy-taxing pathway. Accordingly, the majority of findings has associated an impaired PPT with a reduced "obligatory" energy output (i.e., the energy costs associated with nutrient processing). More recently, it has been reported that "facultative" thermogenesis [e.g., the energy costs associated with sympathetic nervous system (SNS) stimulation] may also contribute to any impairment in PPT among individuals with prediabetes and T2D. Further longitudinal research is required to truly ascertain whether meaningful changes in PPT manifest in the prediabetic state, before the development of T2D.

Phosphorus ingestion with a high-carbohydrate meal increased the postprandial energy expenditure of obese and lean individuals.

OBJECTIVES: Phosphorus ingestion with glucose was reported to stimulate the postprandial peripheral uptake of both phosphorus and glucose, a process that favors energy production. The aim of this study was to determine whether phosphorus ingestion with a meal can affect energy metabolism. METHODS: Overnight fasted men (eight lean and seven obese) consumed a high-carbohydrate meal (648 kcal) with either placebo or phosphorus (500 mg) tablets in a random order. Energy expenditure and substrate oxidation were monitored for 240 min using ventilated hood indirect calorimetry. RESULTS: Phosphorus ingestion with a meal increased the postprandial energy expenditure of both lean and obese individuals (P < 0.001), although in different patterns. Alterations in postprandial substrate oxidation was highly noticeable from time 120 min onward, where phosphorus-treated lean participants exhibited a significant decrease in respiratory quotient. CONCLUSION: Phosphorus ingestion with a high-carbohydrate meal alters postprandial energy metabolism mainly by enhancing postprandial energy expenditure that may ultimatly favor weight loss.

Effects of Moderate Chronic Food Restriction on the Development of Postprandial Dyslipidemia with Ageing.

Ageing is a major risk factor for the development of metabolic disorders linked to dyslipidemia, usually accompanied by increased adiposity. The goal of this work was to investigate whether avoiding an excessive increase in adiposity with ageing, via moderate chronic food restriction (FR), ameliorates postprandial dyslipidemia in a rat model of metabolic syndrome associated with ageing. Accordingly, we performed an oral lipid loading test (OLLT) in mature middle-aged (7 months) and middle-old-aged (24 months) Wistar rats fed ad libitum (AL) or under moderate FR for 3 months. Briefly, overnight fasted rats were orally administered a bolus of extra-virgin olive oil (1 mL/Kg of body weight) and blood samples were taken from the tail vein before fat load (t = 0) and 30, 60, 90, 120, 180, and 240 min after fat administration. Changes in serum lipids, glucose, insulin, and glucagon levels were measured at different time-points. Expression of liver and adipose tissue metabolic genes were also determined before (t = 0) and after the fat load (t = 240 min). Postprandial dyslipidemia progressively increased with ageing and this could be associated with hepatic ChREBP activity. Interestingly, moderate chronic FR reduced adiposity and avoided excessive postprandial hypertriglyceridemia in 7- and 24-month-old Wistar rats, strengthening the association between postprandial triglyceride levels and adiposity. The 24-month-old rats needed more insulin to maintain postprandial normoglycemia; nevertheless, hyperglycemia occurred at 240 min after fat administration. FR did not alter the fasted serum glucose levels but it markedly decreased glucagon excursion during the OLLT and the postprandial rise of glycemia in the 24-month-old rats, and FGF21 in the 7-month-old Wistar rats. Hence, our results pointed to an important role of FR in postprandial energy metabolism and insulin resistance in ageing. Lastly, our data support the idea that the vWAT might function as an ectopic site for fat deposition in 7-month-old and in 24-month-old Wistar rats that could increase their browning capacity in response to an acute fat load.

Effect of food intake on the ventilatory response to increasing core temperature during exercise.

Food intake increases metabolism and body temperature, which may in turn influence ventilatory responses. Our aim was to assess the effect of food intake on ventilatory sensitivity to rising core temperature during exercise. Nine healthy male subjects exercised on a cycle ergometer at 50% of peak oxygen uptake in sessions with and without prior food intake. Ventilatory sensitivity to rising core temperature was defined by the slopes of regression lines relating ventilatory parameters to core temperature. Mean skin temperature, mean body temperature (calculated from esophageal temperature and mean skin temperature), oxygen uptake, carbon dioxide elimination, minute ventilation, alveolar ventilation, and tidal volume (VT) were all significantly higher at baseline in sessions with food intake than without food intake. During exercise, esophageal temperature, mean skin temperature, mean body temperature, carbon dioxide elimination, and end-tidal CO2 pressure were all significantly higher in sessions with food intake than without it. By contrast, ventilatory parameters did not differ between sessions with and without food intake, with the exception of VT during the first 5 min of exercise. The ventilatory sensitivities to rising core temperature also did not differ, with the exception of an early transient effect on VT. Food intake increases body temperature before and during exercise. Other than during the first 5 min of exercise, food intake does not affect ventilatory parameters during exercise, despite elevation of both body temperature and metabolism. Thus, with the exception of an early transient effect on VT, ventilatory sensitivity to rising core temperature is not affected by food intake.