Dairy consumption energy intake and body weight

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Dairy consumption has been associated with both increased and decreased energy intake. A greater consumption of dairy products was associated with a higher energy intake of adults in Bogalusa, LA (Ranganathan et al., 2005). Because an association was also found between the number of servings of dairy products and saturated fat intake, these results suggest that the higher energy intake results from the consumption of high fat dairy products. Surprisingly, the association between dairy consumption and body weight of the study group was not reported. However, Rajpathak and colleagues (2006) found that American men (Health Professionals Follow-up Study) who increased dairy consumption over 12 years gained slightly more weight than those who reduced intake the most. This association was largely due to the intake of high-fat dairy products because low-fat dairy intake was not associated with body weight change. Nevertheless, weight gain with increased dairy consumption was found to be less than predicted by changes in energy intake in healthy older adults (Barr et al., 2000), suggesting greater energy efficiency with dairy consumption. This might be particularly true during periods of rapid growth, such as childhood and adolescence. Phillips and colleagues (2003) found no relationship between higher dairy intake and BMI z-scores or percent body fat in adolescent girls.

In contrast, a link between increased dairy product consumption and healthier body weight has been suggested in several reports. An inverse association has been reported between ready-to-eat breakfast cereal consumption and the BMI of 4-12-year-old children (Albertson et al., 2003) and between the number of servings of dairy products and body fat in pre-school children (Carruth and Skinner, 2001). Similarly, in a large multi-center, population-based, prospective observational study, the number of dairy servings consumed was inversely related to the ten-year cumulative incidence of obesity and to the insulin resistance syndrome in adults (Pereira et al., 2002).

The association between increased dairy product consumption and healthier body weights has been attributed to several milk components, including conjugated linoleic acid (Wang and Jones, 2004), medium-chain triglycerides (St-Onge and Jones, 2003), and particularly calcium (Heaney et al., 2002; Zemel, 2004). Surprisingly, the role of milk proteins has received little attention, despite the fact that protein makes up a major fraction of milk and is the most satiating among the three macronutrients (Anderson and Moore, 2004).

In the following, evidence is presented to show that the consumption of dairy products or their components has a positive effect on satiety and leads to a reduction in energy intake. In order to provide background for establishing plausibility for the associations between dairy products and reduced food intake, a brief review of food intake regulation is provided.

The effects of dairy components on food intake and satiety 21 2.3 The regulation of food intake

Food intake is regulated in both the short and long term by a complex and redundant physiological system that involves a cross-talk between the periphery and the central nervous system (CNS) (Aziz and Anderson, 2006). Although distinct, the pathways controlling short- and long-term food intake overlap in the CNS where they are integrated, orchestrated, and translated into either the suppression or the stimulation of food intake (Schwartz et al., 2000).

2.3.1 The long-term regulation of food intake

Over the long term, the hypothalamus regulates food intake in response to hormones that enter the brain from the peripheral circulation and whose plasma concentrations are related to adipose tissue mass (Schwartz et al., 2000). The two major hormones that have been implicated in the long-term regulation of food intake are leptin and insulin (Badman and Flier, 2005). However, it has recently been shown that ghrelin, a hormone secreted by specialized cells in the stomach, also meets the criteria for a long-term regulator of food intake (Cummings, 2006). Leptin is a hormone arising from adipose tissue and its plasma concentrations are directly proportional to the adipose tissue mass. Although insulin does not arise from adipose tissue, its concentration in blood at fasting and after food ingestion is influenced by adipose tissue mass. It has been proposed that both insulin (Biddinger and Kahn, 2006) and leptin (Munzberg and Myers, 2005) resistance in the brain lead to increased food intake. In contrast to leptin and insulin, ghrelin concentrations in plasma are inversely related to adipose tissue mass (Cummings, 2006).

The major site of action of the adiposity hormones in the brain is a discrete hypothalamic region called the arcuate nucleus (ARC) (Schwartz et al., 2000; Cummings, 2006). Functional receptors for these hormones are expressed in the ARC. Despite the differences in leptin's and insulin's signalling pathways, both hormones elicit an increase in the expression of anorexigenic (appetite-suppressing) neuropeptides and a decrease in that of orexigenic (appetite-stimulating) neuropeptides (Schwartz et al., 2000). On the other hand, the actions of ghrelin in the ARC are opposite to those of leptin and insulin (Cummings, 2006). The major anorexigenic neuropeptides are the pro-opiomelanocortin/a-melanocyte stimulating hormone (POMC/a-MSH) and the cocaine-amphetamine related transcript (CART), whereas the major orexigenic neuropeptides are Neuropeptide Y (NPY) and Agouti related protein (AgRP) (Schwartz et al., 2000). Neurons expressing these neuropeptides project to neighbouring hypothalamic nuclei, particularly the paraventricular nucleus (PVN), ventromedial (VMH), dorsomedial (DMH), and lateral hypothalamus (LH) where they modulate the expression of other sets of anorexigenic (corticotropin releasing hormone (CRH) and thyrotropin stimulating hormone (TSH)) and orexigenic (melanin concentrating hormone

(MCH) and the orexins (ORX A and B)) neuropeptides (Schwartz et al., 2000). Ultimately, the activity of these neurons is translated into the modulation of energy intake and expenditure.

2.3.2 The short-term regulation of food intake

The short-term regulation of food intake encompasses both satiation and satiety. Satiation describes the physiological factors that terminate a meal, whereas satiety refers to the time interval between two meals (de Graaf et al., 2004). Although the energy content of the meal ingested is a major determinant of short-term food intake, it has been increasingly acknowledged that both meal size and meal frequency differ according to the macronutrient composition of the meal (Anderson, 1994).

Short-term food intake is controlled primarily by extra-hypothalamic regions of the CNS, specifically, by the brainstem that receives and integrates neural (vagal) and endocrine signals from the gastrointestinal (GI) tract (Badman and Flier, 2005). The absence of the blood-brain barrier from certain circumventricular organs of the brainstem, such as the nucleus of the tractus solitarius, allows circulating hormones to directly exert their actions on short-term food intake independent of the vagus nerve (Ganong, 2000).

The GI tract is the major organ that generates satiety signals in response to the ingestion of food (Badman and Flier, 2005). The complex and partly autonomous enteric nervous system, along with the plethora of specialized entero-endocrine cells, allows the gut to play a major role in the regulation of food intake. Digestive processes have evolved from the simple role of degradation of macronutrients into their absorbable units to the more complex interactions between macronutrients and the gut in the generation of satiety signals and the regulation of gastric kinetics. Therefore, the GI tract is at the interface between the food and the internal milieu and regulates the generation of satiety signals arising from food, both pre- and post-absorptively.

Pre-absorptive satiety signals

Pre-absorptive satiety signals are generated by the actions of food in the gut lumen and can be classified into endogenous or exogenous gut signals. Endogenous gut signals include mechano-, osmo- and chemo-receptors, but most importantly peptide hormones that are released by specialized endocrine cells in response to food ingestion (Anderson, 1994). Many gut hormones have been identified to date, including cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and bombesin (Strader and Woods, 2005). Among the gut hormones involved in food intake regulation, only ghrelin has been shown to stimulate appetite (Badman and Flier, 2005). Interestingly, most of these hormones and their receptors are also expressed in brain areas such as the hypothalamus in addition to the hindbrain, emphasizing their importance in the control of food intake (Strader and Woods, 2005).

The regulation of the synthesis and secretion of gut hormones is complex, varies across species, and depends on both the macronutrient composition of the diet and other neuroendocrine factors. For example, fat is the major stimulant of CCK release in humans, probably due to the role of CCK in bile acid secretion (Liddle et al., 1985), whereas protein is its most potent stimulant in rats (Liddle et al., 1986). Furthermore, carbohydrates and fats are more powerful GLP-1 secretagogues than protein (Brubaker and Anini, 2003), although protein might enhance the GLP-1 secreting actions of the other macronutrients (Blom et al., 2006; Lejeune et al., 2006).

Exogenous gut satiety signals arise from dietary proteins. These have a hormone-like effect and are able to activate, at the level of the gut, satiety signalling pathways. Commonly referred to as bioactive peptides (BAP) (Kitts and Weiler, 2003), these intermediate products of protein hydrolysis can bind to and activate hormone receptors in the lumen of the gut and induce satiety. For example, BAP that have been shown to have a direct effect on food intake suppression via receptors are opioid-like peptides released during the digestion of casein (casomorphins), soy and wheat gluten proteins (Froetschel et al., 2001; Pupovac and Anderson, 2002).

In addition to their direct effect on hormone receptors, BAP directly or indirectly stimulate the secretion of endogenous gut hormones. Indirect stimulation occurs when dietary peptides act as substrates for intestinal peptidases, thereby sparing hormone-releasing luminal factor from digestion (Liddle, 1995; Wang et al., 2002). Also, BAP can directly stimulate the release of gut hormones from entero-endocrine cells. For example, glycomacropeptide (GMP), a glycolsylated form of caseinomacropeptide (CMP), the first product of digestion of casein, and hydrolysates of b-conglycinin, a major protein in soy, have been shown to be potent CCK secretagogues (Brody, 2000; Nishi et al., 2003a and b). Because BAP are inherent to dietary proteins and can suppress food intake by either stimulating satiety gut hormone release or acting as satiety hormones themselves, they could explain, at least in part, why protein is at the top of the satiety hierarchy of macronutrients.

Table 2.1 shows the major peptide hormones involved in food intake regulation.

Post-absorptive satiety signals

Absorbed nutrients, their metabolites, and some of the hormones involved in their metabolic processes constitute the post-absorptive satiety signals. Theories of feeding have been proposed based on each class of macronutrient: the glucostatic, the aminostatic, and the lipostatic theory of feeding (Anderson, 1994). However the role of changes in blood concentrations of glucose, amino acids, or lipids after a meal in determining either satiation or satiety has been difficult to define.

The fat and carbohydrate metabolites, ketones, lactate, and pyruvate have been proposed to play a role in food intake regulation. Only very high

Table 2.1 Major peptide hormones involved in food intake regulation

Long-term (origin)

Short-term (origin)


Leptin (adipose tissue)

CCK (GI tract)

Insulin (pancreas)

GLP-1 (GI tract)

POMC/a-MSH (hypothalamus)

PYY (GI tract)

CRH (hypothalamus)

Opioid (dietary BAP)

TRH (hypothalamus)

Insulin (pancreas) Leptin (adipose tissue)


Ghrelin (GI tract) NPY (hypothalamus) AgRP (hypothalamus) MCH (hypothalamus) ORX (hypothalamus)

Ghrelin (GI tract)

Note: abbreviations are the following: AgRP: agouti related protein; CCK: cholecystokinin; CRH: corticotrophin releasing hormone; GI: gastrointestinal; GLP-1: glucagon-like peptide-1; MCH: melanin concentrating hormone; MSH: melanocyte stimulating hormone; NPY: neuropeptide Y; ORX: orexins; POMC: pro-opiomelanocortin; PYY: peptide YY; TRH: thyrotropin releasing hormone

Note: abbreviations are the following: AgRP: agouti related protein; CCK: cholecystokinin; CRH: corticotrophin releasing hormone; GI: gastrointestinal; GLP-1: glucagon-like peptide-1; MCH: melanin concentrating hormone; MSH: melanocyte stimulating hormone; NPY: neuropeptide Y; ORX: orexins; POMC: pro-opiomelanocortin; PYY: peptide YY; TRH: thyrotropin releasing hormone concentrations of ketones, such as those observed during starvation or high fat, low carbohydrate diets, are associated with suppression of hunger and appetite (Havel et al., 1999; Freedman et al., 2001). In the fed state, lactate concentrations are increased in proportion to the carbohydrate content of the meal and thus could contribute to the suppression of food intake occurring after carbohydrate ingestion (Havel et al., 1999). Pyruvate, an intermediate metabolite of glucose, glycerol and glucogenic amino acids, is at the center of the hepatic hypothesis of feeding that suggests that hepatic receptor discharges, which cause hyperphagia, are inversely related to the concentration of some key metabolite in the liver (Racotta et al., 1984). In addition, because the liver is the first organ that processes nutrients after their absorption from the gut, it has been postulated that this organ plays an important role in the regulation of the satiety response, either through the presence of receptors or by interacting with the vagus nerve (Novin et al., 1985).

A direct role for absorbed nutrients and their metabolites in intake regulation is difficult to define because their utilization is tightly linked to the release and function of many hormones involved in food intake regulation. For example, insulin and glucagon are released in response to carbohydrate and amino acid ingestion and play a role in short-term regulation of food intake (Anderson, 1994). Although insulin is involved in the long-term control of feeding, it is also directly and indirectly involved in short-term regulation of food intake. Insulin plays a role in the availability of glucose and amino acids to cells, including those in the brain, and in directing the interaction between nutrient ingestion and the action of satiety peptides such as CCK and food intake (Figlewicz et al., 1986).

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