Eating patterns are increasingly varied. Typical breakfast, lunch, and dinner meals are difficult to distinguish because skipping meals and snacking have become more prevalent. Such eating styles can have various effects on cardiometabolic health markers, namely obesity, lipid profile, insulin resistance, and blood pressure. In this statement, we review the cardiometabolic health effects of specific eating patterns: skipping breakfast, intermittent fasting, meal frequency (number of daily eating occasions), and timing of eating occasions. Furthermore, we propose definitions for meals, snacks, and eating occasions for use in research. Finally, data suggest that irregular eating patterns appear less favorable for achieving a healthy cardiometabolic profile. Intentional eating with mindful attention to the timing and frequency of eating occasions could lead to healthier lifestyle and cardiometabolic risk factor management.T he patterns of meal and snack eating behavior in American adults have changed over the past 40 years. Based on NHANES (National Health and Nutrition Examination Survey) data from 1971 to 1974 to 2009 to 2010 (n=62 298), women 20 to 74 years of age reported a decrease in 24-hour meal-derived total energy intake (TEI) from 82% in the 1970s to 77% in 2009 to 2010 and an increase in the proportion of TEI consumed from snacks from 18% to 23%.1 Similar trends were reported among men. The proportion of men and women who reported consuming all 3 standard meals declined over this period (from 73% to 59% in men; from 75% to 63% in women), 1 reflecting changes in eating patterns rather than changes in eating frequency. Indeed, the traditional breakfast-lunch-dinner pattern was not observed in a population of healthy, non-shift-working adults. 2 In that study, the number of eating occasions, defined as consumption of any food or beverage providing at least 5 kcal, was ≈4.2 times a day in the lowest decile and 10.5 times a day for the top decile. There were only 5 hours during the 24-hour day when <1% of all eating occasions occurred: between 1 and 6 am. This study clearly demonstrated that adults in the United States eat around the clock. Because feeding and fasting entrain clock genes, which regulate all aspects of metabolism, meal timing can have serious implications for the development of cardiovascular disease (CVD), type 2 diabetes mellitus, and obesity. 3,4 The circadian rhythms of the body are controlled by the central clock located in the suprachiasmatic nucleus of the hypothalamus but also by clocks of peripheral organs. Although the master clock is strongly entrained by light, clocks of peripheral organs are additionally responsive to food supply, and temporal restriction of food can reset clock gene rhythms. In mice, food given in the normal sleeping period can uncouple peripheral clocks from the master clock. 5 In fact, time-restricted feeding CLINICAL STATEMENTS AND GUIDELINESin mice alters the robustness and coherence of rhythmic gene transcripts, 6 which may be relevant for cardiom...
Highlights d 4-and 6-h time-restricted feeding regimens were tested in adults with obesity d Both regimens produce similar weight loss over the 2 months of the study d Both regimens reduce energy intake by 550 kcal per day without calorie counting d Both regimens produce similar reductions in insulin resistance and oxidative stress
A main function of white adipose tissue is to release fatty acids from triacylglycerol for other tissues to use as an energy source. While endocrine regulation of lipolysis has been extensively studied, autocrine/paracrine regulation is not well understood. Here, we describe the role of AdPLA, the newly identified major adipocyte phospholipase A2, in the regulation of lipolysis and adiposity. AdPLA null mice have a markedly higher rate of lipolysis, due to increased cAMP levels arising from the marked reduction in adipose PGE2 that binds the Gαi-coupled receptor, EP3. AdPLA null mice have drastically reduced adipose tissue mass and triglyceride content, with normal adipogenesis. They also have higher energy expenditure with higher fatty acid oxidation within adipocytes. AdPLA deficient ob/ob mice remain hyperphagic but lean, with increased energy expenditure, yet have ectopic triglyceride storage and insulin resistance. AdPLA is a major regulator of adipocyte lipolysis and critical for the development of obesity.
OBJECTIVETo investigate the role of desnutrin in adipose tissue triacylglycerol (TAG) and fatty acid metabolism.RESEARCH DESIGN AND METHODSWe generated transgenic mice overexpressing desnutrin (also called adipose triglyceride lipase [ATGL]) in adipocytes (aP2-desnutrin) and also performed adenoviral-mediated overexpression of desnutrin in 3T3-L1CARΔ1 adipocytes.RESULTSaP2-desnutrin mice were leaner with decreased adipose tissue TAG content and smaller adipocyte size. Overexpression of desnutrin increased lipolysis but did not result in increased serum nonesterified fatty acid levels or ectopic TAG storage. We found increased cycling between diacylglycerol (DAG) and TAG and increased fatty acid oxidation in adipocytes from these mice, as well as improved insulin sensitivity.CONCLUSIONSWe show that by increasing lipolysis, desnutrin overexpression causes reduced adipocyte TAG content and attenuation of diet-induced obesity. Desnutrin-mediated lipolysis promotes fatty acid oxidation and re-esterification within adipocytes.
Time-restricted feeding (TRF), a key component of intermittent fasting regimens, has gained considerable attention in recent years. TRF allows ad libitum energy intake within controlled time frames, generally a 3-12 hour range each day. The impact of various TRF regimens on indicators of metabolic disease risk has yet to be investigated. Accordingly, the objective of this review was to summarize the current literature on the effects of TRF on body weight and markers of metabolic disease risk (i.e., lipid, glucoregulatory, and inflammatory factors) in animals and humans. Results from animal studies show TRF to be associated with reductions in body weight, total cholesterol, and concentrations of triglycerides, glucose, insulin, interleukin 6, and tumor necrosis factor-α as well as with improvements in insulin sensitivity. Human data support the findings of animal studies and demonstrate decreased body weight (though not consistently), lower concentrations of triglycerides, glucose, and low-density lipoprotein cholesterol, and increased concentrations of high-density lipoprotein cholesterol. These preliminary findings show promise for the use of TRF in modulating a variety of metabolic disease risk factors.
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