Omega-3 and omega-6 essential fatty acids help regulate cholesterol and blood clotting and control inflammation in the joints, tissues, and bloodstream.
Fats also play important functional roles in sustaining nerve impulse transmission, memory storage, and tissue structure. More specifically in the brain, lipids are focal to brain activity in structure and in function. They help form nerve cell membranes, insulate neurons, and facilitate the signaling of electrical impulses throughout the brain. Figure 4. Did you know that up to 30 percent of body weight is comprised of fat tissue? Some of this is made up of visceral fat or adipose tissue surrounding delicate organs.
Vital organs such as the heart, kidneys, and liver are protected by visceral fat. The composition of the brain is outstandingly 60 percent fat, demonstrating the major structural role that fat serves within the body. You may be most familiar with subcutaneous fat, or fat underneath the skin. This blanket layer of tissue insulates the body from extreme temperatures and helps keep the internal climate under control. It pads our hands and buttocks and prevents friction, as these areas frequently come in contact with hard surfaces.
It also gives the body the extra padding required when engaging in physically demanding activities such as ice- or roller skating, horseback riding, or snowboarding. The dietary fats in the foods we eat break down in our digestive systems and begin the transport of precious micronutrients.
By carrying fat-soluble nutrients through the digestive process, intestinal absorption is improved. This improved absorption is also known as increased bioavailability. Fat-soluble nutrients are especially important for good health and exhibit a variety of functions. Vitamins A, D, E, and K—the fat-soluble vitamins—are mainly found in foods containing fat.
Some fat-soluble vitamins such as vitamin A are also found in naturally fat-free foods such as green leafy vegetables, carrots, and broccoli. These vitamins are best absorbed when combined with foods containing fat. Fats also increase the bioavailability of compounds known as phytochemicals, which are plant constituents such as lycopene found in tomatoes and beta-carotene found in carrots. Phytochemicals are believed to promote health and well-being. As a result, eating tomatoes with olive oil or salad dressing will facilitate lycopene absorption.
Other essential nutrients, such as essential fatty acids, are constituents of the fats themselves and serve as building blocks of a cell. When products such as grain and dairy are processed, these essential nutrients are lost.
Manufacturers replace these nutrients through a process called enrichment. Remember, fat-soluble nutrients require fat for effective absorption. For your next snack, look for foods that contain vitamins A, D, E, and K. Do these foods also contain fat that will help you absorb them? If not, think of ways to add a bit of healthy fat to aid in their absorption. Fat-rich foods naturally have a high caloric density.
Foods that are high in fat contain more calories than foods high in protein or carbohydrates. As a result, high-fat foods are a convenient source of energy. For example, 1 gram of fat or oil provides 9 kilocalories of energy, compared with 4 kilocalories found in 1 gram of carbohydrate or protein. Depending on the level of physical activity and on nutritional needs, fat requirements vary greatly from person to person.
When energy needs are high, the body welcomes the high-caloric density of fats. For instance, infants and growing children require proper amounts of fat to support normal growth and development. If an infant or child is given a low-fat diet for an extended period, growth and development will not progress normally. Steroid hormones are insoluble in water, and they are transported by transport proteins in blood.
As a result, they remain in circulation longer than peptide hormones. For example, cortisol has a half-life of 60 to 90 minutes, while epinephrine, an amino acid derived-hormone, has a half-life of approximately one minute. The amino acid-derived hormones are relatively small molecules that are derived from the amino acids tyrosine and tryptophan, shown in Figure Examples of amino acid-derived hormones include epinephrine and norepinephrine, which are synthesized in the medulla of the adrenal glands, and thyroxine, which is produced by the thyroid gland.
The pineal gland in the brain makes and secretes melatonin which regulates sleep cycles. The structure of peptide hormones is that of a polypeptide chain chain of amino acids. The peptide hormones include molecules that are short polypeptide chains, such as antidiuretic hormone and oxytocin produced in the brain and released into the blood in the posterior pituitary gland. This class also includes small proteins, like growth hormones produced by the pituitary, and large glycoproteins such as follicle-stimulating hormone produced by the pituitary.
Figure Secreted peptides like insulin are stored within vesicles in the cells that synthesize them. They are then released in response to stimuli such as high blood glucose levels in the case of insulin. Amino acid-derived and polypeptide hormones are water-soluble and insoluble in lipids. These hormones cannot pass through plasma membranes of cells; therefore, their receptors are found on the surface of the target cells. An endocrinologist is a medical doctor who specializes in treating disorders of the endocrine glands, hormone systems, and glucose and lipid metabolic pathways.
An endocrine surgeon specializes in the surgical treatment of endocrine diseases and glands. Endocrinologists are required to assess patients and diagnose endocrine disorders through extensive use of laboratory tests.
Many endocrine diseases are diagnosed using tests that stimulate or suppress endocrine organ functioning. Blood samples are then drawn to determine the effect of stimulating or suppressing an endocrine organ on the production of hormones. For example, to diagnose diabetes mellitus, patients are required to fast for 12 to 24 hours.
They are then given a sugary drink, which stimulates the pancreas to produce insulin to decrease blood glucose levels. RESULTS: Recent data in the literature shed new light to explain the effects of both leptin and adiponectin in the regulation of lipid metabolism in peripheral tissues.
Activation of the AMP-dependent kinase pathway and subsequent increased fatty acid oxidation seems to be the main mechanism of action of these hormones in the regulation of lipid metabolism. In addition, we have found that insulin plasma levels are positively associated to leptin but negatively correlated with adiponectin in obese children. Adiponectin is negatively associated to plasma lipid markers of metabolic syndrome but positively related to HDL-cholesterol, whereas insulin and leptin show opposite patterns.
These results support the effect of adiponectin in increasing insulin sensitivity and decreasing plasma triglycerides. Adiponectin appears to be the missing link to explain the alterations in lipid metabolism and plasma lipids seen in obesity.
Obesity is characterized by an altered balance between energy intake and energy expenditure. Energy homeostasis is accomplished through a highly integrated and redundant neurohumoral system that minimizes the impact of short-term fluctuations in energy balance on fat mass.
Some of these CNS targets stimulate food intake and anabolic pathways, promoting weight gain, whereas others reduce food intake and catabolic pathways, promoting weight loss. Obesity is associated to the metabolic syndrome characterized by hyperinsulinemia, glucose intolerance or diabetes type 2 and two or more of the following factors: hypertension, hypertriglyceridemia, decreased plasma levels of HDL-cholesterol HDL-c , small and dense LDL particles, increased apoprotein B apo-B , decreased apoprotein A-I apo-A-I and alterations of hemostasia.
Changes in leptin, insulin and adiponectin, associated to obesity and their effects on lipid metabolism, may explain the alterations in plasma lipids and other characteristic features of the metabolic syndrome. In this study, we briefly review the relationships of leptin, insulin and adiponectin with obesity and particularly in the regulation of lipid metabolism and plasma lipids. We also provide results about the relationships of those hormones with plasma lipids in prepubertal children.
Insulin and leptin are secreted in direct proportion, and adiponectin in negative proportion, to the size of the adipose mass. These three hormones are key molecules in the regulation of lipid metabolism. During states of positive energy balance, as it occurs in obesity, the adipose mass expands and more leptin and insulin 1 , 4 but less adiponectin are secreted.
These two hormones, as well as adiponectin, also interact with peripheral tissue receptors modulating energy metabolism. Leptin is produced by adipose tissue and considered to be one of the main peripheral signals that regulate food intake, energy expenditure and body weight, by reporting nutritional information to key regulatory centers in the hypothalamus.
These are mediated both directly, through actions on specific tissues, and indirectly, through CNS endocrine and neural mechanisms. Leptin stimulates fatty acid oxidation and glucose uptake and prevents lipid accumulation in non-adipose tissues, which can lead to lipotoxicity and functional impairments.
Studies involving, intrahypothalamically or intravenously, leptin injection, as well as incubation of soleus muscle or cultured muscle cells with leptin, have demonstrated that leptin stimulates fatty acid oxidation in skeletal muscle by activating phosphorylating AMPK. This enzyme potently stimulates fatty acid oxidation in muscle by inhibiting phosphorylating acetyl-CoA carboxilase ACC activity, which inhibits malonyl-CoA synthesis, activating carnitine palmitoyl transferase 1 CPT1 activity.
These findings demonstrate that AMPK plays a role not only in the alteration of metabolic pathways in muscle and liver but also in the regulation of feeding, and identify AMPK as a novel target for anti-obesity drugs. Although AMPK inactivation in the hypothalamus is puzzling, this finding could be pointing out to the actual role of diet-induced obesity hyperleptinemia.
Weight gain begins when the caloric balance becomes positive, but, ultimately, weight reaches a plateau, indicating that caloric balance has been restored; this equilibrium of caloric intake and expenditure may reflect the action of endogenous hyperleptinemia on the hypothalamus.
Model for the mechanism of action of insulin on fatty acid oxidation in muscle and on hypothalamus in the control of energy intake. There is a controversy about the direct interaction between leptin and insulin.
Apparently, hyperinsulinemia promotes fat deposition, which subsequently increases leptin expression. These results led to the suggestion that leptin might be the signal from adipocytes to islets to hypersecrete insulin when fat content is increased and insulin sensitivity is lowered. It is well known that insulin actions are mainly mediated by phosphatidyl inositolkinase PI-3K , which influences mitogenesis, glucose uptake by GLUT4 transporter and protein phosphatase, which mainly affects glucogen synthesis and lipogenesis.
Adiponectin is an adipose tissue-derived hormone that has an important role as a modulator of insulin action and exhibits anti-inflammatory and antiatherogenic properties. Adiponectin increases insulin sensitivity by enhancing tissue fat oxidation, which results in reduced circulating fatty acid levels and TG contents in liver and muscle.
Model of the interactions of insulin and adiponectin in the control of energy expenditure and lipid metabolism in muscle. However, cholesterol was slightly lower in the obese group. Moreover, HDL-c levels were significantly reduced in obese children compared with the control group.
However, no major differences were observed for apo-A-I. Insulin and leptin were markedly higher in the obese group who developed an insulin resistance pattern, whereas adiponectin was significantly reduced compared with the control children. A high positive and significant correlation was observed between insulin and TGs and apo-B plasma levels, whereas the correlation was negative for HDL-c.
The same pattern was observed for the relationships between leptin and plasma lipids, except that no correlation was found for leptin and apo-B. Absolute values for the correlations between adiponectin and plasma lipids were higher than those obtained for insulin and leptin Table 1. Insulin and leptin were positively correlated, whereas insulin and adiponectin showed a negative association Figure 3.
Although leptin is related to the control of body composition and energy expenditure in animals and humans, the tissue resistance observed in obese subjects explains the observed high plasma levels of leptin without a concomitant inhibition of food intake. Leptin has been shown to be associated to insulin by other investigators in childhood and adult life. Insulin resistance and an altered plasma lipid pattern are common pathophysiological features of the metabolic syndrome not only in adults but also in childhood and adolescence.
Adiponectin seems to be the missing link between insulin resistance and the alterations observed in plasma lipids. In the present study, obese children exhibited a marked hyperinsulinemia, which was positively associated with plasma lipid markers of cardiovascular disease and metabolic syndrome, that is, high levels of TGs and apo-B, but negatively associated with HDL-c and plasma adiponectin concentrations.
Those associations were similar to or higher than those observed for insulin. Moreover, insulin and adiponectin were highly but negatively correlated. From these results, we suggest that adiponectin may have a direct impact in the regulation of insulinemia as well as in lipoprotein metabolism, confirming that, not only in adults but also in prepubertal children, insulin and adiponectin are antagonist hormones reciprocally regulated.
Low levels of adiponectin would decrease the interaction with its hepatic and skeletal muscle receptors and contribute to downregulate the insulin transduction signal cascade, resulting in a reduced fatty acid oxidation, activation of hepatic gluconeogenesis and reduced glucose uptake in both tissues.
Signals that regulate food intake and energy homeostasis. Science ; : — Marx J. Cellular warriors at the battle of the bulge.
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