Osteopetrosis in obese female rats is site-specifically inhibited by physical training.

Serum cholesterol, lecithin-cholesterol acyltransferase, and hepatic hydroxymethylglutaryl coenzyme A reductase activities of lean and obese Zucker rats

Growth hormone (GH) secretion is markedly blunted in obesity. Reportedly, genetically obese Zucker rats show a reduced GH secretion due to an impaired function of hypothalamic neurons producing the GH-releasing hormone (GHRH). The aim of this work was: (1) to compare the in vitro GH responsiveness to GHRH in genetically obese female versus male Zucker rats and, (2) to evaluate the function of hypothalamic GHRH and somatostatin and of pituitary receptors for these neurohormones as assessed by the effectiveness of GHRH and somatostatin on adenylate cyclase (AC) activity. Baseline GH secretion of pituitaries obtained from male and female obese rats was not different and similar to that present in lean counterparts. Stimulation with 10(-7) M GHRH elicited a significantly lower GH secretion from the pituitaries of obese male rats but induced a similar GH secretion from the pituitaries of lean and obese female rats. In these pituitaries, GH concentration was similar in obese versus lean male and female rats [corrected]. A sex-related difference was also evidenced when plasma concentrations of somatomedin C (IGF-I) were evaluated. Obese male rats had lower IGF-I concentrations than lean counterparts, while this was not the case for obese versus lean female rats. Evaluation of AC activity following GHRH disclosed a lower activation in obese than in lean male rats, whereas in the females the enzyme activation was higher in obese than in lean animals. Conversely, the inhibitory effect of somatostatin on forskolin-stimulated AC was similar in pituitary membranes of obese and lean rats of both sexes.(ABSTRACT TRUNCATED AT 250 WORDS)

The present study investigated the effects of moderate physical training on some of the parameters in the GH-IGF axis in experimental diabetic rats. Male Wistar rats were allocated into the following groups: sedentary control, trained control, sedentary diabetic, trained diabetic. Diabetes was induced by alloxan (32 mg/kg, b.w. iv). The physical training protocol consisted of 1 h swimming session/day, 5 days/week for 8 weeks supporting a load corresponding to 90% of maximal lactate steady state. After the experimental period, blood was collected to measure serum glucose, insulin, triglycerides, albumin, insulin-like growth factors-I (IGF-I), and growth hormone (GH). Pituitary gland was removed for GH quantification. Diabetes increased blood glucose and triglycerides and decreased insulin, IGF-I, serum and pituitary GH. Physical training decreased glucose and triglycerides, and also counteracted the reduction of serum IGF-I in diabetic rats. In conclusion, physical training recovered serum IGF-I showing no alteration of serum or pituitary GH levels.

Response of adult lean and obese female Zucker rats to food restriction and refeeding

Comparative studies on fatty acid synthesis, glycogen metabolism, and gluconeogenesis by hepatocytes isolated from lean and obese Zucker rats

Thyroid and Growth Responses of Young Zucker Obese and Lean Rats to a Low Protein-High Carbohydrate Diet

This study presents an in-depth analysis of the effects of obesity on energy balance (EB) and fuel utilization in adult female rats, over the estrous cycle and immediately after surgical ovariectomy (OVX), to model pre- and postmenopausal states, respectively. Female Wistar rats were fed a high-fat (46%) diet for 16 wk to produce mature lean and obese animals. Stage of estrous was identified by daily vaginal lavage, while energy intake (EI), total energy expenditure (TEE), and fuel utilization were monitored in a multichamber indirect calorimeter and activity was monitored by infrared beam breaks. Metabolic monitoring studies were repeated during the 3-wk period of rapid OVX-induced weight gain. Component analysis of TEE was performed to determine the nonresting and resting portions of energy expenditure. Obesity was associated with a greater fluctuation in EB across the estrous cycle. Cycling obese rats were less active, expended more energy per movement, and oxidized more carbohydrate than lean rats. The changes in EB over the cycle in lean and obese rats were driven by changes in EI. Finally, OVX induced a large positive energy imbalance in obese and lean rats. This resulted primarily from an increase in EI in both groups, with little change in TEE following OVX. These observations reveal a dominant effect of obesity on EB, fuel utilization, and activity levels in cycling rats, which has implications for studies focused on obesity and EB in female rodents.

Obesity-related cardiovascular complications are a major health problem worldwide. Overconsumption of the Western diet is a well-known culprit for the development of obesity. Although short-term weight loss through switching from a Western diet to a normal diet is known to promote metabolic improvement, its short-term effects on vascular parameters are not well characterized. Glucagon-like peptide 1 (GLP-1), an incretin with vasculoprotective properties, is decreased in plasma from patients who are obese. We hypothesize that obesity causes persistent vascular dysfunction in association with the downregulation of vascular glucagon-like peptide 1 receptor (GLP-1R). Female Wistar rats were randomized into three groups: lean received a chow diet for 28 wk, obese received a Western diet for 28 wk, and reverse obese received a Western diet for 18 wk followed by 12 wk of standard chow diet. The obese group exhibited increased body weight and body mass index, whereas the reverse obese group lost weight. Weight loss failed to reverse impaired vasodilation and high systolic blood pressure in obese rats. Strikingly, our results show that obese rats exhibit decreased serum levels of GLP-1 accompanied by decreased vascular GLP-1R expression. Weight loss recovered GLP-1 serum levels, however GLP-1R expression remained downregulated. Decreased Akt phosphorylation was observed in the obese and reverse obese group, suggesting that GLP-1/Akt signaling is persistently downregulated. Our results support that GLP-1 signaling is associated with obesity-related vascular dysfunction in females, and short-term weight loss does not guarantee recovery of vascular function. This study suggests that GLP-1R may be a potential target for therapeutic intervention in obesity-related hypertension in females.NEW & NOTEWORTHY Although short-term weight loss successfully improved metabolic parameters, it failed to correct vascular dysfunction present in obese female rats. Vascular GLP-1/Akt signaling was decreased in both obese rats and those with short-term weight loss, suggesting it may be a potential target for therapeutic intervention in obesity-related persistent vascular dysfunction in obese females.

Dietary flaxseed reduces Myocardial Ischemic Lesions, improves cardiac function and lowers cholesterol levels despite the presence of severe obesity in JCR:LA-cp Rats

Sex Differences in Renal Nitric Oxide Synthase, NAD(P)H Oxidase, and Blood Pressure in Obese Zucker Rats

Grier, TL, Canham-Chervak, M, Anderson, MK, Bushman, TT, and Jones, BH. Effects of physical training and fitness on running injuries in physically active young men. J Strength Cond Res 31(1): 207-216, 2017-The purpose of this investigation was to determine the effects of physical training (PT) and fitness on risks for running-related injuries (RRIs) in physically active young men. Personal characteristics, PT, Army Physical Fitness Test scores, and injury data were obtained by survey. Army Physical Fitness Test variables (push-ups, sit-ups, and 2-mile run) were converted into quartiles (Q), where Q1 = lowest performance and Q4 = highest performance. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using multivariate logistic regression. Over 4,000 (n = 4,236) soldiers were surveyed. Running injury incidence was 14%. A greater risk of an RRI was associated with older age (OR31+/<22 years = 1.62, 95% CI, 1.21-2.18), higher BMI ((Equation is included in full-text article.)), and total distance ran per week during unit PT (OR16.1+/1-5 miles = 1.66, 95% CI, 1.15-2.41). A lower risk of an RRI was associated with total distance run per week during personal PT (OR5.1-10/1-5 miles = 0.70, 95% CI, 0.53-0.91, OR10.1-16 +/1-5 miles = 0.58, 95% CI, 0.35-0.97, OR16.1+/1-5 miles = 0.54, 95% CI, 0.30-0.98), higher aerobic endurance as measured by 2-mile run performance (ORQ4/Q1 = 0.50, 95% CI, 0.35-0.72), and unit resistance training ≥3 times a week (OR≥3 times per week/none = 0.46, 95% CI, 0.29-0.73). Greater personal PT running mileage decreased injuries in this population suggesting that the increased protective effect of higher aerobic fitness outweighed the injurious effect of running more miles during personal PT. Countermeasures to prevent RRIs could entail enhancing aerobic endurance, providing opportunities for personal aerobic training, monitoring for excessive unit PT running mileage and encouraging unit resistance training ≥3 times per week.

To determine the relative rates of glycogenesis and lipogenesis following administration of a test meal in lean and obese Zucker rats. Nine-week-old lean and obese Zucker rats were fasted overnight, then tube-fed a test meal of balanced composition amounting to 16kJ (lean rats and one group of obese rats) or 24kJ (one group of obese rats) and containing 200 mg 1-(13)C glucose. Immediately after the meal the rats were injected intraperitoneally with 5 mCi of 3H2O and killed 1 h later. Glycogenesis was calculated from the incorporation of 3H into liver glycogen divided by the specific activity of plasma water. Lipogenesis was calculated similarly from the incorporation of 3H into saponifiable lipids in liver and perirenal adipose tissue. The proportion of glycogen synthesized by the indirect pathway via pyruvate was determined from the ratio of 3H labelling at positions C6 and C2 in the glycogen glucose residues. Glycogen synthesis from glucose was determined from the ratio of 13C enrichment in liver glycogen to that in plasma glucose. The rate of synthesis of glycogen was considerably lower in the livers of obese rats than those of lean controls, with the larger meal causing a small but significant increase in glycogenesis. The proportion of glycogen synthesized via pyruvate showed a non-significant increase in the obese rats, while the amount of glycogen synthesized from glucose was significantly decreased. Hepatic lipogenic rates were about five times higher in both groups of obese rats than the lean controls. In adipose tissue, lipogenesis per g tissue was slightly reduced in the obese rats, although there was clearly an increase in adipose tissue lipogenic activity per whole animal. The larger meal caused a greater rise in plasma glucose and insulin concentrations but did not affect lipogenic rates, although it did cause a greater suppression of lipolysis, as indicated by a lower plasma glycerol concentration. Ingested carbohydrate is partitioned predominantly into hepatic fatty acid synthesis in obese Zucker rats. Hepatic glycogen synthesis is suppressed and comes mainly from precursors other than glucose. The suppression of hepatic glycogen synthesis may contribute to the increased energetic efficiency of obese Zucker rats.

As part of a long-term safety study the bisphosphonate ibandronate was investigated for its effects on bone quality in lumbar vertebrae in rats. Bone area, bone density and mechanical properties were assessed by peripheral quantitative computed tomography (pQCT), dual-energy X-ray absorptiometry (DXA) and compression tests. Female and male groups of Wistar rats received either vehicle or 3, 7 or 15 mg/kg per day of ibandronate over 104 weeks orally by gavage. Compared with the control group, bone mineral density, compressive strength and stiffness were significantly higher in ibandronate-treated animals, whereas no changes occurred in strain or modulus of elasticity. The increase in vertebral body stress was significant in some of the ibandronate-treated groups. The changes in mechanical properties appear to be due mainly to an increase in bone mass. A highly significant correlation was found between bone mineral density measured either by DXA (r = 0.86) or pQCT (r = 0.85) and maximal strength in vertebral bodies (p < 0.0001 each). In conclusion, we demonstrated that lifelong administration of doses of ibandronate far in excess of any therapeutically intended dose not only increases bone mass and apparent density, but also maintains or even slightly improves bone quality. Bone mineral density measured either by pQCT or DXA can be used as a predictor for ultimate strength in rat lumbar vertebral bodies after treatment with ibandronate.

Robust empirical evidence supports the effectiveness of physical and cognitive training in preventing and delaying cognitive decline. Emerging research suggests distinct neurobiological mechanisms underpin the effects of these different training modalities. An unresolved question is whether the mechanisms through which these training modalitiesimpart their effect interact synergistically to improve cognitive outcomes, rather than exerting additive effects, differ. In addition, past research has been inconsistent in adequately controlling for or documenting the dosage of physical and/or cognitive training. Consequently, the aim of this study is to assess the relative effectiveness of physical and cognitive training conducted in isolation or concurrently, whilst rigorously controlling and documenting the treatment parameters. This study is a three-arm randomised controlled trial conducted over a 3-month period, comparing cognitive training, physical activity, and a combination of both interventions. Older cognitively healthy participants (n = 126) aged 60-75years will be recruited from the community. The physical only training will require participants to cycle on a cycle ergometer at above 60% of their age-predicted heart rate maximum for 50min with a 3-min warm-up and cool-down period. The cognitive only training will require participants to complete up to five different cognitive tasks selected from a set of eight on the BrainHQ platform during each 50-min training session. The concurrent cognitive and physical training will require participants to undertake both treatments at the same time. Primary outcomes, assessed pre- and post- intervention, will include speed of processing and episodic memory assessed with the NIH Toolbox, as well as general driving skills assessed on a driving simulator. Findings will inform the design of interventions and population health advice aimed at mitigating cognitive decline. If a substantial synergetic effect is detected, it may lead to the use of more widespread concurrent physical and cognitive training and the potential development of methods to make concurrent training practical. Findings will also provide important clarification as to the relative benefit of the two modes of training. Prospective registration with Australia and New Zealand Clinical Trial Registry (ACTRN12624001088538) on 10th September 2024 and World Health Organisation International Clinical Trials Registry (U1111-1280-3851).

In order to solve the problem of observing the effect of rehabilitation physical training on basketball player injury, a kind of observation study on the effect of rehabilitation physical training on basketball player injury based on memory ultrasound examination was proposed. This study makes a comprehensive analysis of physical fitness training factors such as physical fitness test plan, training arrangement, training method, training monitoring, and effect evaluation. Through the experiment, it is found that there are still gaps in physical training, diagnostic standards, training plans and requirements, load monitoring, standardization of operation, nutrition, and recovery in the training organization. There are only 23.81% of full-time physical coaches and 25.40% of professional team doctors at all levels of sports teams. There were only 23.81% of full-time physical fitness coaches and 25.40% of professional team doctors in all levels of sports teams. Basketball players in the basketball injury survey had 67 sports injuries throughout the year, with a rate of 3.35 injuries per person and 2.48 injuries per 1000 hours. The location of chronic injuries is usually the lower back, knee joint, and ankle. The main injuries are due to the physical component, with injuries occurring most frequently throughout the training season in July, August, and September. Experiments show that good and professional physical training can reduce the risk of injury to a greater extent than strengthening the specific skills of athletes.