Determining the role of omega3 fatty acids and other polyunsaturated fatty acids in weight control

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The positive effects of omega-3 PUFAs were observed early on among Greenland Inuits, who, despite high fat intake, displayed low mortality from coronary heart disease (Dyerberg et al., 1975). Other epidemiological studies have reported lower prevalence of obesity, type 2 diabetes and cardiovascular diseases in populations consuming large amounts of omega-3 PUFAs from fatty fish (Mouratoff et al., 1969; Kromann and Green, 1980). Subsequent studies have demonstrated that dietary supplementation of omega-3 PUFAs exerts positive effects in several metabolic diseases including coronary heart disease, hypertension, arteriosclerosis, diabetes and inflammatory diseases (Terry et al., 2003; Din et al., 2004; Calder, 2004; Ruxton et al., 2004).

13.2.1 Definition, structure and metabolism

The PUFAs are fatty acids containing two or more double bonds. These fatty acids are essential since they cannot be produced in the human body and must therefore be provided in the diet. There are two main types of PUFA, the omega-3 and the omega-6 fatty acids. In the omega-3 PUFAs, the first double bond is located between the third and the fourth carbons, counting from the methyl end of the carbon chain; in the omega-6 PUFA the double bond is located between the sixth and the seventh carbons (Fig. 13.1).

Animals cannot, in general, produce omega-3 or omega-6 fatty acids since they lack the enzymes needed for insertion of the double bonds, whereas in plants these fatty acids are produced via A12- and A15-desaturase activity. The simplest members of the omega-6 and omega-3 fatty

Omega-3 fatty acids and other polyunsaturated fatty acids 283 A

Linoleic acid (18:2n-6 ) CH3

Arachidonic acid (20:4n-6 ) CH3

a-Linolenic acid (18:3n-3 )

CH3 ^COOH

Eicosapentaenoic acid (EPA) (20:5n-3 ) CH3

Docosahexaenoic acid (DHA) (22:6n-3 ) CH3

Fig. 13.1 Schematic structures of common (A) omega-6 and (B) omega-3

PUFAs.

acids are linoleic acid (18:2n-6) and a-linolenic acid (18:3n-3), respectively (Fig. 13.1). Although mammalian cells do not synthesise linoleic acid and a-linolenic acid, these fatty acids are metabolised by desaturation and elongation reactions (Fig. 13.2). Linoleic acid is converted into y-linolenic acid (18:3n-6), which in turn can be elongated to produce arachidonic acid (20:4n-6) (Fig. 13.2). The same group of enzymes have the ability to metabolise a-linolenic acid and convert it into eicosapentaenoic acid (EPA; 20:5n-3). There is thus a competition between the omega-6 and the omega-3 fatty acids in the enzymatic reactions and also for their metabolisa-tion. The A6-desaturase reaction is the rate-limiting step, and this enzyme has a-linolenic acid as its preferred substrate. In the next reaction step, EPA can be further converted through elongation to docosahexaenoic acid (DHA; 22:6n-3) (Fig. 13.2). These long-chain, more unsaturated forms of linoleic acid and a-linolenic acid are in turn substrates for the production of important biological molecules, which will be discussed later in this chapter.

Linoleic acid (18:2n-6 ) a-Linolenic acid (18:3n-3 )

&6-Desaturase

■y-Linolenic acid (18:3n-6 ) Stearidonic acid (18:4n-3 )

Elongase

Dihomo-y-linolenic acid (20:3n-6 ) Eicosatetraenoic acid (20:4n-3 )

&5-Desaturase

Arachidonic acid (20:4n-6 ) Eicosapentaenoic acid (EPA) (20:5n-3 )

Elongase

Docosapentaenoic acid (DPA)(22:5n-3 ) Elongase

24:5n-3

A6-Desaturase 3

24:6n-3

P-Oxidation

Docosahexaenoic acid (DHA) (22:6n-3 )

Fig. 13.2 Metabolic pathways for conversion of linoleic acid and a-linolenic acid into longer derivatives in mammalian cells.

13.2.2 Dietary sources

The different forms of the PUFAs are found in different food sources (Table 13.1). Plant seed oils like corn oil, sunflower oil and safflower oil are rich in omega-6 PUFAs, constituting up to 75% of the fatty acid content. Most plant oils are richer in omega-6 PUFAs than in omega-3 PUFAs (Table 13.2). Sunflower and safflower oil exist in two different forms, one rich in monounsaturated fat and one rich in PUFAs. Linoleic sunflower oil is available as liquid oil and it is also used in margarine. Because of the high levels of PUFAs in these oils, they are susceptible to oxidation during commercial usage, especially frying, and so they are hydrogenated to a more stable form. Thus, important dietary sources of omega-6 PUFAs are the vegetable oils and margarines. Green plant tissues are rich in a-linolenic acid (18:3n-3), constituting more than 50% of the fatty acids. This is, however,

Table 13.1 Food sources of different omega-3 and omega-6 PUFAs

Type of PUFA

Structure

Source

Omega-3

a-Linolenic acid

Walnuts, flaxseed oil, canola oil

EPA

Fatty fish, fish oil

DHA

Fatty fish, fish oil

Omega-6

Linoleic acid

Corn, safflower, soybean and sunflower oil

y-Linolenic acid

Seed oils of borage, blackcurrant and

evening primrose

Arachidonic acid

Meat, eggs

Table 13.2 PUFA content in vegetable oils

Vegetable oil

y-Linoleic acid (n-6) a-Linolenic acid (n-3)

Canola oil

29.6

20.3

9.3

Corn oil

54.7

53.5

1.2

Flaxseed oil

66

12.7

53.3

Safflower oil

74.6

74.6

0

Soybean oil

57.9

51.1

6.8

Sunflower oil

65.7

65.7

0

not a significant source of omega-3 PUFAs since the total fat content is very low (Table 13.3). a-Linolenic acid is abundant in plant oils derived from flaxseed, soybean and rapeseed (Table 13.2). The longer forms of omega-3 PUFAs are more readily found in fatty fish like salmon, herring and mackerel, but also are also found in lean fish liver - which contains large amounts of EPA and DHA (Table 13.3). Nuts contain considerable amounts of omega-3 PUFAs and walnuts, in particular, are rich in a-linolenic acid (Feldman, 2002).

The composition of dietary fatty acids has changed over the last 100 years (Simopoulos, 1995). The total intake of fat and the amount of saturated fats have increased as well as the omega-6 PUFAs, while the intake of omega-3 PUFAs has decreased. Studies in Palaeolithic nutrition suggest that the hunter-gatherer populations consumed equal amounts of omega-6 and omega-3 PUFAs (Eaton et al., 1998). Today the ratio between these fatty acids is 10-20:1 in the Western diet (Simopoulos, 1999). The reason for the decreased intake of omega-3 PUFAs is mainly a reduced intake of fish. In fact, modern agriculture results in decreased omega-3 PUFA content in many foods - including vegetables, meats, eggs and even in cultured fish -due to the industrial production of animal feed with high contents of omega-6-rich grains (Crawford, 1968, Simopoulos, 1999). The increased amount of omega-6 compared with omega-3 PUFAs in standard diets may have

Table 13.3 Food sources of omega-3 fatty acids

Source Omega-3 fatty acid

Seafood

Mackerel 1.8-5.3

Herring 1.2-3.1

Salmon, tuna, trout 0.5-1.6

Halibut 0.4-0.9

Plaice, flounder, haddock 0.2 Nuts and seeds

Almonds 0.4

Flaxseed 22.8

Peanuts 0.003

Walnuts, black 3.3

Walnuts, English 6.8 Vegetables

Broccoli (raw) 0.1

Lettuce 0.1

Radish seeds 0.7

Seaweed, Spirulina (dried) 0.8

Soybeans, green (raw) 3.2

Soybeans, mature seeds 2.1 sprouted

Spinach (raw) 0.1

profound effects on human health since studies have indicated that omega-6 PUFAs may shift the physiological status into a prothrombotic, proaggre-gatory status with increased vasoconstriction and decreased bleeding time (Calder, 2005). The omega-3 PUFAs on the other hand seem antiinflammatory, antithrombotic and hypolipidaemic, and may thus have beneficial effects in the prevention and/or treatment of several metabolic diseases (Calder, 2005).

The dietary PUFA intake is rather similar throughout Western societies. In Sweden and Finland the PUFAs represent around 5% of the total energy consumption (Becker, 1999, Valsta, 1999) and in the United States the intake averages 7%. The omega-3 PUFAs represent ~0.7% of the energy intake, mainly deriving from intake of vegetable oils. The ratio of omega-6 and omega-3 fatty acids is thus approximately 10 : 1 (Kris-Etherton et al., 2000). The dietary sources of PUFAs are mainly vegetable oils and linoleic acid is the major form, constituting 84-89%, while around 10% are represented by a-linolenic acid. The intake of highly unsaturated PUFAs, like the EPA and DHA found in fatty fish, is low, being 0.1-0.65 g/day in the United States. In the United Kingdom the pattern is similar with increasing consumption of linoleic acid (omega-6) and an estimated omega-3 intake of 0.1-0.5 g/day (Sanders, 2000). However, in Malaysian adults the eating pattern is different. The total fat intake range is 22-26%, while in Western countries it is 35-40%, and the PUFAs constitute only around 4% of the fats. The PUFAs consumed are mainly omega-6 linoleic acid and the omega-6 : omega-3 ratio is approximately 10, similar to that in Europe and the United States (Tkw, 1997).

13.2.3 Food intake and body weight control

High-fat food intake is considered to be one of the major causes of the development of obesity and obesity-associated insulin resistance (Astrup, 2001; Riccardi et al., 2004). Laboratory animal studies and epidemiological studies in humans have demonstrated that consumption of high-fat dense diets, a typically Western diet, results in insulin resistance and obesity (Storlien et al., 2000; Astrup, 2001; Winzell and Ahren, 2004). There are however, studies indicating that different types of fat have different effects on whole-body energy metabolism and glucose homeostasis, and inclusion of dietary oils containing PUFAs have been proposed to exert positive effects both in patients and in animal models of type 2 diabetes (Malasanos and Stacpoole, 1991; Storlien et al., 1991). There are studies demonstrating that PUFAs, in particular the omega-3 PUFAs (EPA and DHA), are less effective in promoting obesity compared with saturated fats (Shillabeer and Lau, 1994; Azain, 2004). The mechanisms behind these observations probably involve modulation of fuel partitioning since PUFAs down-regulate lipogenesis and stimulate fat oxidation, because these fatty acids regulate the expression of several genes involved in lipid metabolism (Clarke, 2004; Sampath and Ntambi, 2004). Reduction in body fat content has been observed in rodents fed a diet containing fish oil (Ruzickova et al., 2004; Ikemoto et al., 1996), demonstrating that omega-3 PUFAs decreased the visceral fat by inhibiting both hypertrophy and hyperplasia of the fat cells.

In contrast, the effect of omega-3 PUFA on human body weight control is rather limited. However, in a recent study, overweight men and women were assigned to a daily fish meal, a weight-loss programme or the two in combination for 16 weeks and the effects on body weight and the plasma glucose and lipid profile were investigated (Mori et al., 1999). The fish meal did not in itself reduce the body weight of these obese subjects, but the dietary fish component significantly improved the outcome of the weight-loss programme in that body weight was reduced in combination with improved glucose and insulin levels as well as the serum lipid profile. In another study, 17 subjects (healthy, obese and type 2 diabetic) entered a 5-week diet programme with diets rich in either saturated fats or PUFAs (Summers et al., 2002). Both energy and fat intake appeared to be reduced in the subjects on the PUFA-rich diets, although body weight was not altered. The abdominal subcutaneous fat area was reduced in the group consuming the PUFA-rich diet, and this coincided with improved insulin sensitivity. The results indicate that PUFAs are effective in altering body fat content, which may have beneficial effects on energy metabolism.

13.2.4 Clinical studies on the effect of polyunsaturated fatty acids on glucose control and dyslipidaemia

The effect of omega-3 fatty acids on glycaemic control in humans is controversial. Several studies and reviews have indicated that omega-3 PUFAs have adverse effects in that these fatty acids induce elevated basal plasma glucose, and this was particularly pronounced in patients with type 2 diabetes consuming large amounts of fish oil (>10 g fish oil/day) (Borkman et al., 1989; Friday et al., 1989; Vessby, 1989). However, in other studies with lower doses of omega-3 PUFAs, ranging from 1-2 g/day, glucose homeostasis was maintained within normal ranges (Westerveld et al., 1993; Luo et al., 1998; Sirtori et al., 1998). Luo et al. (1998) demonstrated that a moderate intake of omega-3 PUFAs (1.8 g/day) in type 2 diabetic men resulted in a significant reduction in plasma triglyceride levels. There were, however, no effects on fasting glycaemia or HbA1c. During the 2-month study, body weight and energy intake remained stable. In addition, in other studies, which included patients with hypertension and dyslipidaemia, no adverse effects on plasma glucose levels were observed (Grundt et al., 1995; Toft et al., 1995). In both human and animal studies, dietary omega-3 PUFA supplementation was found to result in reduced circulating triglyceride levels, which may be one explanation for the improved insulin sensitivity observed after fish-oil feeding (Mori et al., 1999; Sirtori et al., 1998). The triglyceride-lowering effect is the most consistent and reproducible finding in both animal and human studies with omega-3 PUFAs and fish oil. Two meta-analyses of trials with omega-3 PUFAs or fish oil in patients with type 1 and type 2 diabetics, as well as in healthy controls, demonstrated that dietary fish oils have no statistically significant effect on glycaemic control but the supplementation efficiently reduced plasma triglyceride levels (Friedberg et al., 1998; Montori et al., 2000). There is thus strong evidence suggesting no adverse effects of fish oil or omega-3 PUFAs on glycaemia, and beneficial effects on plasma lipids, when consumed in moderate doses (1-3 g/day).

Animal studies have demonstrated that various dietary fat subtypes can modulate insulin action indicating that PUFAs have positive effects on insulin sensitivity (Storlien et al., 1991, 2000). One study, where rats were fed isocaloric high-fat diets with different types of fatty acids, demonstrated that diets rich in saturated fat resulted in insulin resistance while rats fed a high level of PUFAs with a low omega-6 : omega-3 ratio had normal insulin action (Storlien et al., 1991). It is thus possible that saturated fatty acids affect the cellular membranes in a negative way resulting in impaired insulin action and that this can be prevented by the addition of unsaturated fatty acids to the diet (Ma et al., 2004). PUFAs may thus, at least in animal models, affect glycaemic control by improving insulin sensitivity.

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