1 Introduction

Obesity is a state of increase in the mass of adipose tissue with concomitant elevation of body weight greater than the levels of physical requirements. Accumulation of triacylglycerols is believed to be the only manner in which body weight has become excessive. However, obesity cannot be simply defined in terms of body weight solely. In that concept, short individuals are supposed to be lighter than tall ones. There is also a need to standardize body weight against height, which is the body mass index (BMI) (equals a person’s weight in kilograms (kg) divided by their height in meters squared (m2)). The World Health Organization (WHO 1985) defined obesity as BMI > 30 for men and BMI > 28.6 for women.

Obesity is seen as a significant global health concern. More than 2 billion people who are equivalent to 30 percent of the global population are obese or overweight (BMI is greater than or equal to 25 kg/m2) (Ng et al. 2014). It is a major health concern because it predisposes subjects to a variety of comorbidities. Accumulation of excess body fat produces an elevated risk for cardiovascular diseases, multiple forms of cancer, increased mortality, type 2 diabetes, stroke, and osteoarthritis (Björntorp 1993; Guh et al. 2009). Recently, there has been tremendous evidence that obesity has a detrimental impact on the brain. Visceral obesity, in particular, is associated with severe metabolic changes in the central nervous system even in younger populations (Kaur et al. 2015). Obesity has also been involved in cognitive deficits in dementia patients (Whitmer et al. 2007).

Obesity etiology is multi-factorial, both genes and environmental factors may be involved. In particular, increased caloric intake and decreased physical activity are the main causes of weight gain (Pereira et al. 2005; Castro et al. 2020). However, there are also secondary reasons for obesity including endocrine disorders and medications (Karam and McFarLane 2007). Also, a deficiency of vitamin D can be a risk factor for obesity (Kaddam et al. 2017).

Currently, the available therapies for obesity have not been able to reduce its prevalence. Diet therapy with increased physical activity does not achieve significant short-term weight reduction (Frood et al. 2013). Besides, current anorexic drugs and surgical procedures have several harmful side effects that may exceed their benefits (Yanovski and Yanovski 2014). The use of adjuvants in current treatments is therefore a novel, safe, and effective strategy.

These ingredients can help to increase the effectiveness of hypocaloric diets by reducing the side effects associated with low energy intake and avoiding the feeling of hunger (Chambers et al. 2014). Many obese individuals tend to eat more foods containing certain functional elements that help to reduce their weight. From these elements, conjugated linoleic acids (CLAs) are known to be antiobesogenic agents in both animals and humans. A variety of studies researched the treatment of CLAs on obesity (den Hartigh et al. 2017; van Baak and Mariman 2019; Namazi et al. 2019).

Medium-chain triglycerides (MCTs) are triglycerides with saturated fatty acids that have a chain length of 6–12 carbons. Beyond their recognized nutritional values, they substantially minimize bodyweight relative to long-chain triglycerides in mice (Zhang et al. 2015; Sung et al. 2018). Clinical research also demonstrated that for obese women, MCTs succeeded in lowering body fat and weight (Krotkiewski 2001). CLAs and MCTs also increased satiety and decreased energy consumption, suggesting a possible role in helping to maintain energy balance (Coleman et al. 2016; Maher et al. 2020).

However, the study of CLAs and MCTs data, concerning their antiobesity effects, is still inconclusive. Hence, the purpose of this article is to summarize the various kinds of literature discussing the effects of CLAs or MCTs on body weight and fat deposition in obese animals or humans. Also, the authors have tried to explore and compare the potential pathways involved in reducing adiposity by both fats. Moreover, the safety of these fat supplements was considered.

2 Adipose tissue and obesity

Fats are stored in adipose tissue, which is classified into anabolic white adipose tissue (WAT) and catabolic brown adipose tissue (BAT). Their roles are different; WAT stores energy as triacylglycerols (TAGs), while the BAT oxidizes lipids to produce energy (Lee et al. 2014). The balance between WAT and BAT is necessary to maintain homeostasis energy. Notably, WAT is considered an endocrine organ that secretes many adipokines with autocrine, endocrine, and paracrine functions. It has a functional diversity that can affect most of the body’s systems. WAT is also primarily produced by adipocytes but there are different types of cells in this tissue, such as stem cells, lymphocytes, macrophages, preadipocytes, and endothelial cells. Therefore, it has the heterogeneity of cells (Ràfols 2014). WAT secretes various lipid substances mainly fatty acids (released under energy deprivation conditions such as in fasting), prostanoids, cholesterol, and vitamin A (Trayhurn 2005). Besides, sex hormones and glucocorticoids are developed by WAT, as it secretes a large number of protein-grade adipokines that have been classified as adipokines such as leptin, resistin, adiponectin, inflammatory, and anti-inflammatory cytokines (Wozniak et al. 2009). However, WAT is distributed across human bodies; Fat deposits are present in the abdomen around the omentum, bowel, and peripheral areas. Subcutaneous fats are also considered to be from the main fat deposits. The locations of WAT determine its metabolic and endocrine properties (Tchkonia et al. 2002). WAT is sensitive to glucocorticoids in the neck and the upper back, meanwhile; it is extremely affected by estrogen in the breasts. Intra-abdominal fat secretes adipokines, which are closely linked to inflammation and type 2 diabetes. Under conditions of excess energy or sedentary life, these deposits are increasing and the production of proinflammatory adipokines has increased with the consequent promotion of atherosclerosis (Yudkin et al. 2005). Obesity is therefore defined as excess body fat associated with a risk of type 2 diabetes and cardiovascular disease depending on the location of excess fat.

3 Causes of obesity

The main causes of weight gain are strongly linked to high-calorie intake and a sedentary lifestyle. Obesity can also be secondary to adverse changes in the neuroendocrine system or genes. Such changes can affect the energy imbalance, appetite, fat distribution, and metabolism of lipids and glucose (Karam and McFarlane 2007). Various secondary factors were included.

3.1 Endocrine disorders

Obesity is associated with many endocrine disorders such as hypothyroidism (Santini et al. 2014), leptin resistance (Sáinz et al. 2015), polycystic ovarian syndrome (Lo et al. 2006), Cushing’s syndrome (Wajchenberg et al. 1995), hypothalamic disorders (Srinivasan et al. 2004), growth hormone deficiency (Rosen et al. 1993), and hypogonadism (Bhasin et al. 2003).

3.2 Vitamin D deficiency

Vitamin D deficiency is documented in obese patients (Kaddam et al. 2017). Vitamin D can contribute to overweight or even obesity through its effects on glucose and fat homeostasis by acting on the pancreas (Delvin et al. 2010). Cell culture and animal studies have shown that adipose tissue has a vitamin D receptor (VDR) and also can synthesize vitamin D in its bioactive metabolite (1,25 dihydroxy vitamin D3).

Vitamin D may increase adipose tissue lipogenesis and adipogenesis (Earthman et al. 2012) which leads to obesity. Cases of vitamin D deficiency have reported higher levels of parathyroid hormone (PTH) (Stein et al. 2009). Hyperparathyroidism has a potential role in obesity by promoting lipogenesis thus encourages weight gain (Snijder et al. 2005). Wakayo et al. (2016) have shown that for a unit elevation in the vitamin D serum level of school children, overweight or obesity risk is reduced by 5.8%. Also, weight loss and decrease in blood androgen levels and blood pressure were fulfilled in obese women who had a significant decrease of vitamin D with polycystic ovarian syndrome after three months of vitamin D supplementation (Pal et al. 2012). It was found that circulatory vitamin D repletion in extremely obese subjects was achieved by the use of prescribed forms of ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3) but the latter is preferable (Stein et al. 2009).

3.3 Genetics

Obesity is a form of polygenic disease. It is the product of the cumulative action of genetic, epigenetic, and environmental influences (Herrera et al. 2011). Several genes have been actively involved in signaling between the hypothalamic satiety and hunger centers and the peripheral leptin, convertase 1, and melanocortin 4 receptors. Mutation of these genes leads to extreme early obesity (Clément et al. 1998).

In particular, insulin and leptin stimulate certain neurons in the hypothalamus to produce alpha-melanocyte-stimulating hormone (alpha-MSH), a neurotransmitter that acts on hypothalamus melanocortin receptors (MCR) to reduce food intake. Mutations of genes responsible for alpha-MSH or MCR contribute to obesity (Girardet and Butler 2014). Moreover, another mutation of genes encoding leptin, leptin receptor, or proopiomelanocortin is associated with weight gain. Human obesity may result from polygenic mutations (Comuzzie and Allison 1998).

3.4 Medications

Side effects of many drugs may develop obesity among susceptible subjects. Antidiabetic medications such as insulin, thiazolidinediones, and sulfonylurea have been shown to increase body weight gain in diabetic patients (Cheng and Kashyap 2011). Also, several therapies that function centrally as antidepressants (Patten et al. 2011), antiepileptics, and antipsychotics may increase body weight gain by operating on brain monoamines (Newcomer and Lieberman 2007).

Besides, the withdrawal of nicotine during smoking cessation was associated with weight gain (Bush et al. 2016). Possible mechanisms include declining metabolic resting rate, decreased physical activity, reduced-calorie burn, and increased appetite.

3.5 Environmental chemicals

Substances such as endocrine-disrupting chemicals (EDCs) may be related to the obesity epidemic (Baillie-Hamilton 2002). Exposure to EDCs takes place at home, in the workplace, on the farm, in the air we breathe, the food we consume, and the water we drink. Early-life exposure to atmospheric particles increases susceptibility to dietary weight gain, insulin resistance, adiposity, and inflammation (Wei et al. 2016). Obesogens are a group of EDCs that may interact with the endocrine system and may contribute to obesity (Janesick and Blumberg 2016).

Bisphenol A (BPA), is used in plastic containers for food and beverage. The composition of BPA is identical to estradiol. Consequently, it binds to estrogen receptors in the body (Do et al. 2017). Phthalates can promote obesity through anti-androgenic effects, anti-thyroid activity, and/or activation of peroxisome proliferator-activated receptors (PPARs) (Kim and Park 2014). Atrazine is an herbicide that is widely used. It has been shown to destroy mitochondria in rats, decrease the metabolic rate, and increase abdominal obesity (Lim et al. 2009). Organotin polluting tributyltin (TBT) contributes to obesity in humans by increasing the number of fat cells (Grün 2014).

3.6 Disruption of energy homeostasis

Continuous disturbance of energy homeostasis contributes to adiposity. The central nervous system (CNS) regulates the feeding activity and thus influences the energy balance. Disturbances in the feeding activity lead to a high incidence of obesity. Energy expenditure includes the basic metabolic rate (BMR), thermogenesis, and physical activity.

BMR is equivalent to about 60–70 percent of the total energy expenditure and it increases with an increase in body weight. However, BMR is centrally regulated (Galgani and Ravussin 2011) that, when dysregulated results in weight gain. It is worth mentioning that physical activity is responsible for 20–30% of overall energy expenditure, except for athletes. A sedentary lifestyle is responsible for major obesity (Bhurosy and Jeewon 2014).

3.7 Saturated and trans-fats

Fats and oils in the diet are the main sources of energy as compared to the other macronutrients. High intake of such fats increases the proportion of calories that would be closely associated with overweight or, in some instances, with obesity (Raatz et al. 2017). It is well documented that a high intake of saturated fatty acids (SFA) is associated with obesity, especially in obesity-prone carriers of the obesity gene (Phillips et al. 2012). Hu et al. (2018) exposed mice to 29 types of diets varying in the proportions of fat, carbohydrates, and protein. They found that increased energy intake and adiposity were caused only by elevated dietary fat content. Astrup (2005) findings are consistent with those of Hu et al. (2018) since they suggested a low-fat diet to avoid weight gain, obesity, type 2 diabetes, and cardiovascular disease. It was found that the degree of saturation of fatty acids affects their β oxidation (Kien et al. 2005). Therefore, SFA increases the deposition of fats in adipose tissue (Piers et al. 2003). In addition to classic monoamine systems and leptin in controlling energy balance, there are two opposing systems, one orexigenic and one anorexigenic, which are part of the energy balance regulation. Neuropeptide Y (NPY) and agouti-related protein (AgRP) are orexigenic, increase food consumption, and enhance obesity. Diets with high saturated fats content significantly increased NPY protein expression with concomitant body weight, elevation (Piggott et al. 2002).

Trans-fats (TFs) are prepared by the hardening of both vegetable and marine oils by industry. Also, trans-fatty acids are naturally constituted a small content in ruminants, meat, and milk. Koh-Banerjee et al. (2003) documented that a high intake of TFs elevated the risk of weight gain and abdominal fat. This could be explained by the role of TFs as ligands for the peroxisome proliferator-activated receptors gamma (PPARγ) system (Mozaffarian et al. 2006) and by induction of insulin resistance (Kavanagh et al. 2007).

4 Dietary supplements and obesity

Lifestyle modifications by changes in diet and physical activity are expected to be the cornerstone of the management of obesity (Strasser and Fuchs 2016). However, people are failing to reach their weight-reduction goals. Therefore, the provision of dietary supplements could be helpful for weight reduction. Many animal studies have shown that high consumption of oleuropein (Lepore et al. 2015) or oleoresin (Lombardo et al. 2018) (olive oil products) is significantly correlated with weight reduction. Merola et al. (2017) also proved that citrolive, a commercial extract from the combination of citrus fruit and olive leaf extracts, could ameliorate the metabolic disorders associated with obesity in rats. In humans, consumption of extra virgin olive oil showed a decline in body weight in obese women (Galvão et al. 2018). Moreover, weight reduction by enhancing lipid metabolism through activation of AMP-activated protein kinase (AMPK) by tea polyphenols has been reported (Rothenberg et al. 2018). Since AMPK can modulate energy homeostasis and lipid metabolism. The results of Yang et al. (2018) are consistent with those of Rothenberg et al. and added that consumption of 600–900 mg tea catechins substantially reduces weight gain. Furthermore, apple polyphenols have anti-obesity effects through a variety of pathways, including free radical scavenging, regulation of gene expression, and altering signal transduction in fat tissues (Asgary et al. 2018). A combination of hibiscus and lemon verbena polyphenolic extracts was consumed by overweight subjects. It exerted an anthropometric measurement improvement, increased anorexigenic hormone (glucagon-like peptide-1), and reduced orexigenic hormone (Ghrelin) through AMPK (Boix-Castejón et al. 2018).

Recently the health benefits of fats may vary according to their fatty acid compositions (Schwab et al. 2014). Fatty acids that consumed in relatively large amounts are linoleic, oleic, and palmitic, meanwhile, others such as α-linolenic acid (ALA), median chain triacyleglycerols, and omega 3 fatty acids are consumed in smaller quantities, but they have clear health benefits (Oliveira-de-Lira et al. 2018) and may be used as dietary supplements (Ludwig et al. 2013).

4.1 Conjugated linoleic acid supplement

Conjugated linoleic acids (CLAs, 18:2n-6) are natural fatty acids found in meat and dairy products. CLAs are isomers of linoleic acid (LA) but with a double-bond conjugated system. Ruminants have an enzyme that converts omega 6 fatty acids in green plants to CLAs that are stored in animals’ meat and milk. They are also present to a lesser degree, in turkeys, chickens, and pigs.

Synthesized CLAs can be also produced by the action of fermentative bacteria in LA (Kishino et al. 2002). CLAs have a variety of beneficial effects on cancer, atherosclerosis, and obesity (Koba and Yanagita 2014; den Hartigh 2019; Basak and Duttaroy 2020; O’Reilly et al. 2020). The most beneficial effect associated with the intake of trans-10, cis-12 CLAs (t10-c12- CLAs) isomer is the reduction of obesity in both animals and humans (den Hartigh et al. 2018; Mądry et al. 2016 respectively). CLAs consumption by obese patients with non-alcoholic fatty liver disease often significantly improves their lipid profile, glycemic response, and markedly ameliorates oxidative stress (Ebrahimi-Mameghani et al. 2016). On the other hand, for overweight type 2 diabetics, the administration of CLAs for eight weeks does not affect anthropometric measurements and body composition (Shadman et al. 2013; Namazi et al. 2019). In the meantime, CLAs supplementation for obese postmenopausal women with type 2 diabetes significantly improves both body weight and glycemic parameters (Norris et al. 2009; den Hartigh 2019). López-Plaza et al. (2013) reported that skimmed milk fortified with 3g of 1:1 mixture of CLAs isomers (c9-t11 and t10-c12) to overweight healthy subjects for 24 weeks significantly decreased both body weight and total fat mass. Also, Kamphuis et al. (2003) documented that a mixture of CLAs isomers increased the feeling of fullness and increased satiety after thirteen weeks of supplementation. A reduced weight gain was achieved after six months of intake of mixed isomer CLAs (Watras et al. 2007). Both t10-c12 CLAs supplementation and diet restriction in mice exerted equal weight reduction with more fat loss by CLAs followed by increased fat oxidation and energy consumption (den Hartigh et al. 2017).

4.1.1 Mechanisms of CLAs

Many studies demonstrated that CLAs exert their effects by influencing lipid metabolism, modifying enzyme activity, and hormonal profile (Kennedy et al. 2010; Lehnen et al. 2015). CLAs isomers significantly increase lipolysis in human adipocytes and diminish fatty acids synthesis (Martins et al. 2015). They also inhibit the expression of genes that are involved in the differentiation of the pre-adipocytes to mature adipocytes thus reducing lipogenesis (Reardon et al. 2012). The peroxisome proliferator-activated receptors (PPARs) are transcription factors in the nucleus that play an important role in the catabolism and the storage of fatty acids. PPARα and β isomers are involved in the expression of proteins responsible for fatty acid oxidation and, PPARγ isomer is associated with adipocytes differentiation (Tavares et al. 2007). CLAs inhibits PPARγ leading to the reduction of body fat by altering the gene expression that inhibits cell differentiation and modulates the activity of proteins involved in lipogenesis and lipolysis (Boschini and Garcia Júnior 2005) (figure 1).

Figure 1
figure 1

Pathways of CLAs for managing obesity.

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PPARγ in the adipocytes regulates the expression of genes of acyl-CoA synthetase, lipoprotein- lipase (LPL), and fatty acid transport protein that is involved in the uptake of fatty acids into the adipocytes (Tavares et al. 2007). As a result, the activation of PPARγ increases acyl-CoA synthetase which activates fatty acids, forming an activated complex with carnitine palmitoyl-transferase-1 (CPT-1). This complex enters the mitochondria where it is oxidized to produce adenosine triphosphate (ATP) (Yamashita et al. 2008).

CLAs increase the activity of CPT-1consequently and collectively reduce the accumulation of fatty acids in the adipose tissue. Increased β oxidation of mitochondrial fatty acids induced by CLAs also significantly decreases triacylglycerols synthesis with concomitant reduction of adipocyte size (Botelho et al. 2005). The reduction of body fat occurred due to a decrease in adipocyte size, not the number.

It is noticed that CLAs significantly elevated the expression of the uncoupling protein of the respiratory chain-1 (UCP-1) that leads to weight loss (Busiello et al. 2015). Where, β oxidation of fatty acids results in energy, part of this energy is used for the production of ATP, the rest of the energy is released as heat. UCP-1 also is known as thermogenin, it accelerates the loss of energy as heat. Thus, CLAs increases energy metabolism and expenditure via increasing basal metabolic rate (BMR) or thermogenesis. Consistent with this theory, Shen et al. (2013) proved that the CLAs increase the browning of white adipose tissue with a concomitant increase in energy expenditure. The increased brown fat is significantly associated with lower obesity risk in both mice (Almind et al. 2007) and humans (Cypess et al. 2009). It has been documented that t10-c12 CLA noticeably elevates cyclooxygenase (Cox-2) expression and production of prostaglandin (PG) in the human adipocytes associated with the induction of browning of WAT (Madsen et al. 2010).

Coelho et al. (2019) demonstrated that dietary fat can regulate obesity through its effects on gut microbiota. Diets supplemented with 0.5 percent t10c12 CLA for eight weeks resulted in enhanced cecum fermentation with the concomitant rise in short-chain fatty acids (SCFAs). The intake of CLAs regulates dysbiosis-induced obesity by gut microbiota modulation (Marques et al. 2015). SCFAs induce satiety through the elevation of circulating anorexogenous hormones (Nilsson et al. 2013) and the reduction of ghrelin in the blood (Parnell and Reimer 2009).

4.1.2 Adverse effects of CLAs

It is noteworthy that some animal and human studies have shown that CLAs administration can increase inflammation and insulin resistance (Risérus et al. 2004; Hamilton et al. 2015; Shen and McIntosh 2016), where cultured adipocytes treated with t10 C12CLA display inflammatory reactions (den Hartigh et al. 2013). Besides, CLAs consumption has been related to reduced insulin signaling in mice (Poirier et al. 2006) which is indicative of insulin resistance. Den Hartigh et al. (2017) confirmed that CLAs supplementation significantly enhances weight loss associated with insulin resistance. These drawbacks in the consumption of CLAs are significantly related to the dose. High levels of t10-c12CLA might increase inflammatory markers (LaRosa et al. 2006). In addition to inflammation, such high doses of CLAs cause an increase in hepatic steatosis that is characterized by an overt appearance of fats in the liver, increased liver weight and triacylglycerol content which may be attributed to insulin resistance (Shen et al. 2013). Therefore, controlling the supplemented level or dose of CLAs is a must.

4.2 Medium-chain triglycerides supplement

Medium-chain triglycerides (MCTs) are esters formed of glycerol and three fatty acids with a chain length of 6–12 carbon atoms. Dietary medium-chain fatty acids (MCFAs) include caproic acid or hexanoic acid (C6:0), caprylic acid, or octanoic acid (C8:0), capric acid, or decanoic acid (C10:0), and lauric acid (C12:0). Natural sources of MCFAs in the form of MCTs are coconut and palm kernel oils. MCTs differ from long-chain triglycerides (LCTs) by their smaller molecular size. Besides, MCTs are hydrolyzed faster and more extensively during digestion. MCFAs also undergo limited re-esterification as they have a low affinity for anabolic enzymes such as diglyceride acyltransferase. Furthermore, after digestion, both MCFAs and MCTs are directly reached into the liver via the portal system for rapid oxidation (Babayan 1987). MCFAs and MCTs efficiently enter the mitochondria without carnitine esterification (Hoppel, 1982) through the CPT-1 transport system. Unlike long-chain fatty acids (LCFAs) which are packed into chylomicrons for their tissue distribution through the lymphatic system, allowing maximum uptake by adipose tissue for storage as fat. Collectively, MCTs are extremely less likely to be stored, don’t produce ectopic fat metabolites which promote insulin resistance and also inflammation (McCarty and DiNicolantonio 2016). MCTs were documented to reduce the accumulation of body fat in both clinical trials and animal studies (Liu et al. 2009; Liu et al. 2012). Also, St-onge and Jones (2002) have shown that MCTs have important potential in the prevention of obesity.

It is well documented that the consumption of MCTs in ad libitum meals can substantially induce satiety and reduce body weight (Rial et al. 2016; Gunasekaran et al. 2017). It was also found that when MCTs were added to human breakfast, the consumption at the next meal was reduced (Van Wymelbeke et al. 1998). In this context, MCTs supplementation reduces energy intake over the following two days compared to long-chain triglycerides. Decreased energy intake may be mediated by increasing β-hydroxybutyrate concentration and/or delaying gastric emptying (Maher et al. 2020). Furthermore, there was reduced intake at the dinner after lunch with MCTs as compared to LCTs or other fat replacements (Van Wymelbeke et al. 2001). Interestingly, MCTs consumption resulted in a decrease in food intake either in overweight males (St-Ong et al. 2014) or in healthy, non-obese adult males (Van Wymelbeke et al. 1998).On the other hand, it has been stated that there is no impact on food intake by MCTs supplement (Poppitt et al. 2010). This controversy may be explained by the small dose of MCTs (10 g) in this study. In the meantime, the effective doses in other studies were 20g or more of MCTs. Obese women eating coconut oil had a marked reduction in waist circumference as compared to those who consumed soya bean oil (Assunção et al. 2009). McCarty and DiNicolantonio (2016) recommended that lauric acid should be administered instead of LCFAs to manage obesity, as it is less obesogenic and does not intensify obesity. In mice, coconut oil reduced body weight gain and decreased fat deposition after six weeks of treatments (Gunasekaran et al. 2017).

4.2.1 Mechanisms of MCTs

Zhang et al. (2015) fed a high-fat diet with 2% MCTs or LCTs to obese mice for twelve weeks. Their results showed that diet-containing MCTs produced a significant reduction in fat mass. Such a decrease may be partially attributed to the activation of BAT, probably by the norepinephrine (NE) pathway. Since MCTs are significantly irritating to the sympathetic nervous system, an increase in expression of mRNA, and the protein of the beta-3adrenergic receptors (β3-AR) was observed. NE can trigger many biochemical lipolysis reactions such as the up-regulation of adipose lipase and hormone-sensitive lipase (Liu et al. 2012). NE may also induce thermogenesis (Zhao et al. 1994). It was proved that an increase in β3-AR expression could cause elevated UCP-1 expression in BAT and thermogenesis (Lowell and Flier 1997).

Very low-calorie diets (VLCD) enriched with MCTs or LCTs have been administered to obese women for 4 weeks. Both body fat and body weight showed a significant reduction in the MCTs’ diet. Moreover, the feeling of hunger was lower and directly proportional to the levels of the plasma ketone bodies. Also, MCTs diet-induced lower nitrogen excretion in the urine (Krotkiewski 2001) indicating a protein-sparing effect of MCTs with a concomitant transition to anabolic protein metabolism. Recently, some studies indicate that the net protein catabolism is decreased by 32% in the ketone state such as in cases of fasting and VLCD conditions (Ryde et al. 1993). In this case, ketones that are the result of fatty acid oxidation are utilized by the brain and skeletal muscles as an energy source (figure 2). Therefore, they ameliorate the hunger feeling, spare protein conversion to glucose, and increase the synthesis of proteins (Hoffer et al., 1982). MCTs produce ketones even in the presence of a large concentration of glycogen (Foster and McGarry 1982) because they have rapid access to the inner mitochondrial matrix in the hepatocytes. The main ketone formed by MCTs is the β-hydroxybutyrate. It decreases appetite and exerts an anorexic effect (Laeger et al. 2010).

Figure 2
figure 2

Mechanism of energy production via dietary MCTs.

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Many obese patients have a variety of metabolic abnormalities with multifactorial causes. Among these factors, the disturbance of gut microbiota is identified as a causative factor for such complications in obese subjects. MCTs supplementation does not only improve this dysbiosis but also improves intestinal permeability, which helps to manage obesity (Rial et al. 2016). Correction of gut microbiota significantly enhances obese well-being and thus increases SCFAs, consequently participates in weight reduction (Parnell and Reimer 2009; Nilsson et al. 2013). Moreover, the influence of MCTs on reduction in satiety and food intake is done by a significant increase of MCFAs in plasma after MCTs consumption such as capric, caprylic, and lauric. These fatty acids affect the acylation mechanism of ghrelin, which modulates the feeling of satiety and appetite (Lemarié et al. 2016). Each of the capric acid and lauric acid promotes fatty acid oxidation with a concomitant increase of satiety (Lemarié et al. 2015). Cholecystokinin (CCK) is the first gut hormone that is found to affect satiety. Ingestion of lipid is linked to the secretion of CCK which depends on the length of the fatty acid chain. It is reported that CCK is considered a mediator of fat-related satiety via delaying gastric emptying (Matzinger et al. 1999). It was noticed that CCK was released after the ingestion of either capric or lauric acids (Mclaughlin et al. 1999). Furthermore, Feltrin et al. (2004) found that C12 and C10 fatty acids increased CCK release, but the magnitude of this elevation was higher with C12.

Dietary administration of MCTs may likely influence mRNA expression of genes capable of altering the lipogenic capacity of animals (Ferreira et al. 2014). MCTs work through PPAR-γ to down-regulate adipogenic genes. Moderate doses of MCTs are required to improve their anti-lipogenic effect otherwise high doses can have lipogenic effects (Marten et al. 2006).

Peptide YY (PYY) is an amino acid peptide that belongs to pancreatic peptides. Its secretion is stimulated by the sense of protein and fats. It has an anorexic effect by inhibiting food intake via increasing the C-fos expression in the arcuate nucleus (ARC). ARC reduces food consumption (Riediger et al. 2004). MCTs containing 56% octanoic and 43% decanoic acid markedly increased PYY secretion (Maas et al. 1998). This finding was supported by Feltrin et al. (2007) since they found that decanoic acid could stimulate the PYY release in a dose-dependent manner. Moreover, in overweight men, MCTs administration significantly elevated the concentrations of leptin and PYY but did not affect ghrelin or GLP-1as compared to LCTs (St-onge et al. 2014).

4.2.2 Adverse effects of MCTs

The MCTs administration as oil may produce a large elevation of plasma ketones which returns to the normal levels within three hours. This can be avoided by the ingestion of intact sources of these MCTs such as coconut oil which causes a less prominent and a delayed rise of ketones (Newport 2013). Also, although MCTs have an important effect on weight loss, they can increase fasting triglycerides and cholesterol levels (Gunasekaran et al. 2017). By contrast, Sung et al. (2018) demonstrated that MCTs have a potential role in lowering the blood lipids in diabetic rats. Also, this hypercholesterolemia can be considered to be benign (McCarty and DiNicolantonio 2016) and can be avoided by administering moderate amounts of such oils (Marten et al.2006). However, it has been shown that MCTs did not have toxicological effects, even with chronic dietary supplementation (Nagao and Yanagita 2010).

5 Conclusion

Obesity is a condition of excessive body weight with an exaggeration of adipose tissue. It plays an important role in several pathophysiological disorders such as atherosclerosis, hypertension, insulin resistance, and diabetes. The etiology of obesity is multifactorial. The primary causes of obesity are higher caloric intake, especially with saturated and/or trans-fats, and a sedentary lifestyle. Meanwhile, secondary factors include several endocrine disorders, vitamin D deficiency, gene mutation, some medications, environmental obesogens, and disruption of energy homeostasis. Many strategies are designed to minimize weight gain; however, each has some adverse effects. Therefore, a trial used a hypocaloric diet with some dietary supplements has shown marked success. Certain dietary fats, besides their role as a source of energy, can be used as nutraceuticals or dietary supplements to enhance weight reduction. In this context, CLAs and MCTs exhibit a promising issue. Several mechanisms are involved to explain their effects such as increasing satiety, energy expenditure, correcting intestinal microbiota, modifying gene expression, reducing food intake, and increasing mitochondrial oxidation. However, their amounts or doses should be carefully adjusted to avoid unpleasant side effects. Further experimental studies and clinical trials are warranted to confirm the use of such fats as complementary medicine with selected a strategy for weight reduction.