Daria Pašalić
Department of Medical Chemistry, Biochemistry and Clinical Chemistry
Zagreb University School of Medicine
Šalata ul 2.
10 000 Zagreb, Croatia
Phone +385 (1) 4590 205; +385 (1) 4566 940
E-mail: dariapasalic [at] gmail [dot] com

Useful links

Short review


Branka Salzer1, Željko Trnka2, Mate Sučić3. Obesity, lipoproteins and physical activity. Biochemia Medica 2006;16(1):37-42.
1Labor Centar, Polyclinic for Medical Biochemistry Diagnosis, Zagreb, Croatia
2Society for Sport Recreation, Zagreb, Croatia
3Department of Internal Medicine, Dubrava Clinical Hospital, Zagreb, Croatia
Obese persons are at a high risk to develop hyperlipoproteinemia, diabetes mellitus, hypertension, coronary disease, and degenerative diseases. Excessive body mass and obesity have numerous and diverse adverse effects on health. Along with many consequences directly influencing the quality of life, there is an increased risk of premature death. The risk factors for cardiac disease include elevated concentration of total and LDL cholesterol, a decreased concentration of HDL cholesterol, increased concentration of triglycerides and blood glucose, elevated arterial blood pressure, cigarette smoking and inadequate physical activity. Disease development can be prevented and delayed by regular physical activity.
Key words: obesity, risk factor, lipoproteins, disease prevention, physical activity
Received: June 16, 2005                                                                                                              Accepted: January 10, 2006
Adverse effects of excessive body mass and obesity on health are numerous and varied; they include increased lipid concentration in the blood, elevated blood pressure, low insulin sensitivity, hypokinesia (insufficient physical activity). In developed countries, obesity is also associated with many psychosocial problems encountered by obese individuals due to stigmatization. Particular attention should be focused on abdominal (visceral, android or male) obesity which has become the topic of investigations during past decades (1). Abdominal obesity has different pathogenetic mechanisms and adverse effects and is related to a much higher health risk than peripheral (female, gynecoid) obesity. Abdominal obesity in men and women is associated with higher rates of mortality, stroke, ischemic heart disease, elevated blood pressure, glucose intolerance, diabetes type 1, and increased concentration of serum lipids.
Definition of obesity and body mass
Obesity is excess of fat tissue in the body reaching a stage when it becomes risk to health. The degreeof obesity and fat tissue distribution in the body may have variable impact on health among individuals. Normal percentage of fat tissue in 18-year-old males is approximately 15–18%, and in 20-year-old women it is 20–25% of the body mass. The percentage of fat tissue usually rises with age. Sexual differences in fat tissue distribution can be observed even in the early years of life. The distribution of fat tissue is in women mostly peripheral (hips and buttocks – gynecoidobesity), and in men mostly central (chest and abdomen – android obesity). Effect of different fat tissue distribution on changes in metabolism becomes evident if the fact that fat tissue metabolism is different in different body parts is taken into consideration. Studies have shown the omentalfat tissue to be more susceptible to catecholamine action than subcutaneous peripheral fat tissue. As catecholamines are the basic lipolytic factors of human lipid cells, the increase in abdominal mass induces enhanced lipolysis (2).
Early differentiation between android and gynecoid obesity is possible by waist-hip measurement ratio (waist measurement in centimeters divided with hip measurement in centimeters). The waist-hip measurement ratio higher than 1 and 0.85 for men and women, respectively, indicates abdominal (android or male) obesity and warns of a high health risk even at slightly increased body mass. Recent data have shown that the waist measurement (taken at the midpoint between the lower rib arch and upper segment of the hip bone) is itself a sufficiently good criterion to indicate risks due to abdominal obesity. By monitoring changes in waist measurement, it is possible to follow up changes in the risk for occurrence of cardiovascular and other chronic diseases (3).
Obesity and lipoproteins
Basic effect of obesity on lipoprotein metabolism is enhanced secretion of lipoproteins containing apolipoprotein B from the liver. The total number of VLDL particles secreted from the liver is elevated in obese individuals. Several factors may stimulate increased formation of VLDL particles in the liver and liver secretion, with enhanced effect of energy substrates in the liver being among the most important ones. This increased formation occurs not only after meals but also during fasting due to increased uptake of free fatty acids secreted in the plasma from increased fat tissue. High concentration of serum free fatty acids results in their increased intake in the liver. This phenomenon is particularly pronounced in visceral obesity, which is more frequent in men than women because increased quantities of free fatty acids directly reach hepatic portal circulation. Increased production of VLDL particles in obese individuals may, but does not have to, cause hypertriglyceridemia. Generally, the level of triglycerides and VLDL particles is higher in obese than in thin individuals, yet the triglyceride level may not necessarily exceed recommended values in the obese. If a person has a relatively low activity of lipoprotein lipase or this activity is not increased with body mass increase, enhanced VLDL and triglyceride formation surpasses the capacity of the lipolytic system and induces an increase in serum triglyceride concentration. The result of such increase is hypertriglyceridemia which is the most frequent disorder of the lipid metabolism in obese individuals. Due to hypertriglyceridemia, these individuals are at increased risk for development of coronary disease (4).
Clinical trials have demonstrated that obesity is also responsible for hypercholesterolemia. This fact may be accounted for by the increased intake of saturated fatty acids and cholesterol, which reduces the activity of LDL-receptor and brings about an increase in LDL-cholesterol level. Another cause is enhanced production of apoprotein B-containing lipoproteins in obese individuals, which enhances VLDL to LDL conversion and increases LDL-cholesterol concentration. Still, it should be emphasized that cholesterolemia is not found in all obese individuals. Further effect of obesity is lowered serum HDL-cholesterol concentration. It seems that low HDL concentration, found in most obese persons, is of two origins. First, the high triglyceride level frequently found in obese individuals reduces HDL-cholesterol concentration. Second, it seems that obesity lowers the concentration of HDL particles independently of the triglyceride concentration, which may be due to enhanced catabolism of HDL particles. Variations in lipoprotein metabolism demonstrated that subcutaneous abdominal adipocytes bind to HDL more actively than omental fatty acids and that HDL binding to adipocytes increases with the size of lipid cells (5). Increased HDL binding to adipocytes is found in obesity, particularly in abdominal subcutaneous area. Reduction in body mass results in decreased HDL binding to lipid cells, which can account for reciprocal increase in HDL-cholesterol concentration found in obese individuals who reduced their body mass (6). Negative correlation has been established between HDL cholesterol and body mass index. Low HDL concentration, which represents particular risk for the development of atherosclerosis, is to some extent related to waist-hip measurement ratio and body mass index. After body mass reduction, HDL concentration may initially decrease but it usually increases; it increases more in men than in women.
When obese individuals begin to reduce their energy intake, their HDL cholesterol may slightly increase, as a result of decline in triglyceride concentration, but HDL cholesterol concentration does not return to normal long after body mass reduction. In general, HDL cholesterol in most obese individuals diminishes from 0.13 to 0.26 mmol (7).
Lipids and physical training
It is debatable whether early physical training involves prevention of the occurrence of obesity, elevated blood lipid concentration, elevated arterial blood pressure and low insulin tolerance. Insufficient physical activity is a risk factor for early atherosclerosis. Risk factors for the occurrence of cardiovascular disease that are affected by physical activity are as follows:
-          body mass that regulates calorie consumption
-          arterial hypertension, with physical activity being one of the measures for hypertension prevention and therapy
-          diabetes mellitus, as the glucose level declines during physical effort
-          smoking and alcohol – desire for smoking and alcohol consumption is lesser in persons who work out and engage in recreational activities
-          stress – recreation reduces stress
-          lipids – physical exercise decreases the concentrations of total cholesterol, LDL-cholesterol, and mostly also of triglycerides, while primarily increasing HDL-cholesterol concentration which protects against atherosclerosis (8, 9).
The causes of increase in HDL-cholesterol concentration are also activities of lipoprotein lipase found mainly in fat tissue and skeletal muscles. Relatively increased lipoprotein lipase in women’s fat and muscle tissue accounts for higher HDL-cholesterol level and lower VLDL concentration. Similarly to heparin injection, regular alcohol consumption causes heightened activity of lipoprotein lipase from the fat tissue, while physical activity enhances the activity of this enzyme from skeletal muscles. In both cases, HDL-cholesterol concentration is elevated (10).
Aerobic exercises (e.g., running, cycling, rowing or swimming) lower the levels of triglycerides, total cholesterol and LDL-cholesterol, and elevate noticeably HDL-cholesterol concentration. These changes depend on intensity of physical activity.
Younger men benefit more from physical activity regarding HDL-cholesterol than the older ones, women benefit less than men, but younger women benefit more than the older ones. The use of contraceptive pills inhibits HDL-cholesterol increase in physically active women. Moderate drinking of alcohol (2 dl wine daily) contributes to HDL-concentration increase in the similar manner as physical activity, while excessive intake of alcoholic beverages elevates triglyceride concentration and exerts harmful effects.
HDL-cholesterol concentration rises during running or swimming. Men and women aged 50–65 years need two years of systematic intense recreation to achieve changes in the lipid status (11).
There have been few reports on HDL-concentration decline during physical activity. Obesity is inversely proportional to the level of physical exercise. Physical activity without reduction diet is seldom sufficient to achieve body mass reduction. Nevertheless, along with body mass reduction, physical exercise allows maintenance or even increase in non-fat body mass, leading to reduced waist-hip measurement ratio which is otherwise related to increased development of coronary disease, diabetes mellitus and arterial hypertension. Physical training also improves glucose tolerance.
Most researchers agree that moderate physical activity is sufficient to reduce individual risk factors. In this regard, regularity, frequency and duration of aerobic activity is more important than its intensity. According to results of studies on effect of physical training in secondary prevention of coronary disease, the tendency of lower morbidity and mortality was observed in regularly active individuals with 300–400 kcal of weekly additional energy consumption during walking, exercises or work of moderate intensity (12).
Secondary prevention of coronary atherosclerosis is based on regular exercise performance and low-calorie diet.
Current opinion is that moderate physical activity, performed regularly during spare time, may not necessarily lead to substantial improvement in body fitness but may be sufficient in primary prevention of coronary disease. In this case, aerobic activity is recommended as it has more substantial impact on changes in risk factors than other types of activities. Aerobic activities that involve action of large muscle groups during a prolonged period are selected according to medical condition and preferences of an individual, i.e. patient (hiking, race walking, swimming, jogging, cycling, etc.) (13).
Primary prevention of coronary disease implies adherence to general recommendations on the type, intensity, duration and frequency of exercise. It is recommended that aerobic activity be 65% of maximum cardiac frequency, i.e. 50% of the maximum oxygen intake during 15–60 minutes three to five times a day. All these exercise guidelines are also determined by individual’s functional status, and every exercise should be composed of initial warming up, gradual introduction of activity and its gradual termination.
It is important to instruct both healthy individuals and particularly patients who are to take part in physical exercise on how to recognize the signs of developing cardiac complications and warn them of the importance of gradual involvement in physical activity.
Participation in physical activity begins with organized and supervised programs in specialized institutions. Each exercise should be preceded by 5–10 minutes of warming up, stretching exercises or walking. The same procedure should be followed also at the end of exercises. Elderly persons should be particularly observant of this rule. The exercises required both in primary and secondary prevention of coronary disease must be moderately pleasant, outlined individually, safe, relaxing, isotonic, controlled and funny in order to minimize withdrawal from training.
Increase in serum cholesterol concentration and blood pressure, obesity, smoking, physical inactivity and diabetes are independent factors that enhance the risk for cardiovascular disease. Presently it is known that the disease incidence could be reduced and its progression retarded by controlling these factors. The control also involves adherence to the low calorie diet with reduced total fat intake (approximately 30% of energy) and promotion of healthy physical activity appropriate to age. It may be concluded that physical activity has significant positive corrective and preventive effect on all the above risk factors, which is the most important conclusion from the aspect of health care.



1.   Nichols AB, Ravenscraft C, Lamphiear DE, Ostrander LD. Independence of serum lipids and dietary habits. The Tecumseh study. JAMA 1976;236:1948-53.

2.   Physical status: the use of interpretation of anthropometry. Report of WHO Expert Committee. World Health Organ Tech Rep Ser 1995;854:368-9.

3.   Cardiovascular disease program. Integrated management of cardiovascular risk. Report of WHO Meeting, Geneva, July 9-12, 2002.

4.   Obesity, preventing and managing of global epidemic. Report of WHO Consultation on Obesity, Geneva, June 3-5, 1997. Geneva: World Health Organization, 1998.

5.   Steffes MW, Gross MD, Schreiner PS, et al. Serum adiponetectin in young adults - interaction with central adiposity, circulating levels of glucose and insulin resistance. The Cardio study. Ann Epidemiol 2004;14:492-8.

6.   Jousilathi P, Tuomilehto J, Vartiainen E, Pekkanen J, Piska P. Body weight, cardiovascular risk factors and coronary mortality. 15-year follow-up of middle-aged men and women. Circulation 1996;93:1372-9.

7.   Fortmann SP, Maron DJ. Disorders of lipid metabolism. In: Rubenstein E, Federman DD, editors. Scientific American Medicine. New York: Scientific American, 1992:9-11.

8.   Young DR, Steinhardt M. The importance of physical fitness for the reduction of coronary artery disease risk factors. Sports Med 1995;19:303-10.

9.   Duraković Z, et al. Tjelesno vježbanje i zdravlje. Zagreb: Grafos d.o.o., 1999.

10. Beier CH, Lisch HJ, Braunsteiner H. Polymorphes Erscheinungsbild der alkoholinduzierten Hyperlipaemie. Dtsch Med Wochenschr 1984;109:1728-9.

11. Fagar RH. Prescription and results of physical activity. J Cardiovasc Pharmacol 1995;25 (Suppl 1):20-7.

12. Buemenn B, Tremblay A. Effects of exercise training on abdominal obesity and related metabolic complications. Sports Med 1996;21:191-212.

13. Kovač M, Strel J, Mišigoj-Duraković M, ed. Telesna vadba in zdravje. Ljubljana: ZDŠPS Fakulteta za šport, 2003.