Obese Strains Research Articles

Carcass, muscle and meat characteristics of lean and obese pigs.

Six pigs obtained from a lean selected strain and six pigs obtained from an obese selected strain were slaughtered at about 110 kg live-animal weight. Carcasses were evaluated; hams were dissected into bone, skin, fat and lean, and loin samples were obtained for fiber type characteristics, percentage of fat and moisture, collagen analysis, sensory characteristics, textural properties and objective color analysis. Carcasses from lean pigs were longer, had less backfat and larger longissimus muscle cross-sectional areas than carcasses obtained from obese pigs. Hams from lean pigs had less fat, more bone and more lean than hams from carcasses of obese pigs. The percentages and cross-sectional areas of red and white muscle fibers of the longissimus muscle from lean and obese pigs were not different. However, lean pigs had intermediate fibers that were only 79% as large (P less than .10) as intermediate muscle fibers from obese pigs. Intermediate fibers represented only 7 and 10% of total fiber area, whereas white fibers represented 84 and 79% of total fiber area in longissimus muscle of lean and obese pigs, respectively. Overall, lean pigs tended to possess fewer fibers (-16%) per unit of area than obese pigs, indicating that total muscle fiber hypertrophy was partially responsible for the increased longissimus muscle area of the lean strain. Sensory properties of longissimus meat samples from lean and obese strains were not different. However, the shear force requirement of the longissimus samples from the lean strain were slightly, but significantly (P less than .10), higher than those from the obese strain. No differences were observed in meat color.

Sera-controlled preadipocyte growth in culture: an ontogeny study with sera from lean and obese pigs.

Genetically lean and obese swine were used to investigate the control of preadipocyte growth in culture by porcine serum. Sera were collected from fetuses from obese and lean strains at 70, 90 and 110 d of gestation. Postnatal serum samples were collected from both lines of pigs at 23 to 27 kg. Rat preadipocytes were isolated and grown in culture. Preadipocyte and stromal-vascular cell proliferation was greater in cultures grown in sera obtained postnatally than in cultures grown in sera from fetuses. Sera from lean and obese fetuses were equipotent in promoting cell proliferation. Glycerol-phosphate dehydrogenase (GPDH) activity was higher in cultures fed serum from obese pigs and fetuses than in cultures fed serum from lean pigs and fetuses. Cultures grown in serum from obese fetuses and pigs had soluble protein levels similar to cultures grown with serum from lean pigs and fetuses. These results demonstrate that serum from genetically obese swine, in the pre-obese (fetal) and obese (postnatal) state, caused increased adipogenic activity in adipocytes in culture.

Enhancement of cold-stimulated thermogenesis in the corpulent rat (LA/N cp) by aminophylline.

Previous studies on obese strains of rats (e.g., Zucker and LA/N cp) have shown that they are deficient in nonshivering thermogenesis and poor in cold tolerance. Our earlier studies have established that aminophylline (AMPY; 85% theophylline-15% ethylenediamine) is effective in significantly improving cold tolerance in the lean Sprague-Dawley rat regardless of age or thermogenic capacity. The present study tested whether AMPY may be also effective in improving cold tolerance in both young (12-18 wk) and older (36-42 wk) lean and corpulent LA/N cp rats. Contrary to previous reports, however, the norepinephrine (NE)-stimulated nonshivering thermogenesis was not only present but also equal in magnitude in the corpulent rats to that of their lean controls. Further, no difference in cold tolerance was observed between the two groups regardless of age. Similarly, AMPY (18.7 mg/kg ip) significantly improved thermogenesis and cold tolerance in both lean and corpulent rats, again without any age-related difference in response. These results indicate that, despite the existence of obesity, no difference in thermogenic capacity to either NE or cold stimulation is evident in the LA/N cp rats. Thus the ontogeny of obesity in this strain may be caused by factors other than deficiency in NE- or cold-stimulated thermogenesis at the end-organ level.

Central, as well as peripheral naloxone administration suppresses feeding in food-deprived sprague-dawley and genetically obese (Zucker) rats

Food intake over 90 min post-injection was studied in groups of food deprived (20 hr) female Sprague-Dawley (S.D.) rats, fatty Zucker (fa/fa) rats and their heterozygous lean litter mates (Fa/fa) of various ages, that bar-pressed for food pellets on a FR-1 schedule following a subcutaneous (SC) or an intracerebroventricular (IVT) injection of sterile saline or naloxone HCl. Subcutaneous injections of naloxone HCl (10 mg/kg) reduced feeding in all three groups of rats compared to SC saline; in addition, a greater percentage reduction in food intake over the whole 90 min test period occurred in the Fa/fa rats given SC naloxone compared to the Fa/fa group. Intracerebroventricular naloxone (50 μg) decreased feeding over the initial 30 min period in the S.D. and Fa/fa rats but a 100 μg IVT dose was needed to reduce feeding in the fa/fa group. The results demonstrate that central naloxone administration can suppress feeding in both non-obese and obese strains of rats as it is known to do when given peripherally. These findings add yet further evidence to the premise that endogenous opioid peptides may play an intricate and important physiological role in the regulation of feeding behavior.

Relation between body fat and glycogen levels of inbred strains of mice.

Previous studies suggested that an inverse relation existed between concentrations of body fat and muscle glycogen among inbred strains of mice. Of six strains, one, the I strain, was resistant to obesity, and the levels of muscle glycogen were 3–6 times greater than those of the other five strains. Because the tentative proposal was based on data from only one lean strain, mice of the DBA strain were studied as another possible lean strain. Although small animals, sublines 1 and 2 of this strain became obese when fed a 50% fat diet, and the levels of muscle glycogen were in the range of the other five obese strains. It was also found that concentrations of body fat up to 25% could be induced in 4–5-month-old mice of the I strain, and by dietary means alone. The concentrations of muscle glucogen in these mice were not lower than those of I strain mice exhibiting concentrations of body fat of 11%. It was concluded, therefore, that an inverse relation between carbohydrate and fat stores does not exist among inbred strains of mice. The unusually high levels of muscle glycogen in the I strain appear to be unique, and are most likely genetically determined.

Muscle and Liver Glycogen Levels in Lean and Obese Strains of Mice

Muscle and liver glycogen concentrations were determined in six strains of inbred mice (A/Fn, C3H/Fn, C57BL/Fn, I/Fn, BUB and Lt) of which only one could be considered to be truly non-obese. This lean strain, the I, showed higher muscle glycogen in both the fed (on either a 5 or 50% fat diet) and fasted states. In contrast to the other strains their muscle glycogen did not readily deplete following a fast. Two of the strains, the Lt and C57, were considered to be moderately obese and under some conditions they showed somewhat higher muscle glycogen levels than the severely obese strains, the A, C3H and BUB, but this pattern was not consistent. Our data suggest that an inverse correlation exists between muscle glycogen and body fat levels in these six mouse strains. Fed liver glycogen concentrations were usually greater in the five obese strains than in the I strain but no consistent pattern was found in the obese strains. These carbohydrate variations suggested endocrine differences among the strains. However, an explanation of these variations in terms of higher or lower titers of any hormone leads only to contradiction when the fat and protein differences of these strains are also considered.

The liver in obesity.

EXPERIMENTAL obesity produced by hypothalamic injury in various species of animals is uniformly accompanied with liver damage, progressing occasionally to cirrhosis.1In hereditarily obese strains of mice, liver damage is also seen uniformly, and even tumors of the liver are observed.2Although the increased incidence in human obesity of gall-bladder disease3and diabetes mellitus4has long been known, and although these conditions may lead independently to liver disease, there does not appear to be in the literature a consideration of the existence of liver damage in obesity per se. The majority of obese persons show a significant decrease in carbohydrate tolerance,5and this impairment has been related to the duration rather than to the degree of obesity.6Similar decreases in carbohydrate tolerance are observed in the experimental obesity of hypothalamic injury1and in hereditarily obese mice.7Newburgh and Conn8suggested that the disturbed carbohydrate metabolism occurring with obesity is related