Excess Calories Research Articles

Childhood obesity: Sequelae in adult life

Childhood obesity is a growing global health hazard extending to adulthood. The prevalence of obesity in children in developed and developing countries has risen dramatically in the past few decades and is currently at epidemic proportions. Obese children and adolescents were around five times more likely to be obese in adulthood than those who were not obese. Adiposity rebound in early childhood is a risk factor for obesity in adolescence and adulthood. Numerous sequelae are associated with children being overweight or obese, even at a very young age. Obesity in childhood and adolescence is significantly associated with an increased risk of insulin resistance, type 2 diabetes mellitus, dyslipidemia, hypertension, metabolic syndrome, non-alcoholic fatty liver disease, and obstructive sleep apnea. Obese children are more likely to experience psychological morbidity, lower self-esteem, and more behavioral problems than non-obese children. These comorbid conditions may progress to adult life and the development of atherosclerosis, cerebrovascular disorders, and cardiovascular morbidity later in life. Obese children are more likely to become obese adults and suffer lifelong physical and mental problems and risk of premature mortality. The use of infant formula, decreased physical activity, excessive calorie intake, and changes in gut microbiota patterns are associated with the increasing prevalence of childhood obesity. Efforts will be focused on trying to treat obesity itself and, therefore, prevent progression to overt sequelae, either in childhood or later in adult life. The most important strategy for preventing obesity and sequelae is lifestyle modification which includes healthy eating behaviors, regular physical activity, and reduced sedentary activity. Bangladesh J Medicine 2023; Vol. 34, No. 2(1) Supplement: 191-192

Impact of short and long exposure to cafeteria diet on food intake and white adipose tissue lipolysis mediated by glucagon-like peptide 1 receptor.

The modern food environment facilitates excessive calorie intake, a major driver of obesity. Glucagon-like peptide 1 (GLP1) is a neuroendocrine peptide that has been the basis for developing new pharmacotherapies against obesity. The GLP1 receptor (GLP1R) is expressed in central and peripheral tissues, and activation of GLP1R reduces food intake, increases the expression of thermogenic proteins in brown adipose tissue (BAT), and enhances lipolysis in white adipose tissue (WAT). Obesity decreases the efficiency of GLP1R agonists in reducing food intake and body weight. Still, whether palatable food intake before or during the early development of obesity reduces the effects of GLP1R agonists on food intake and adipose tissue metabolism remains undetermined. Further, whether GLP1R expressed in WAT contributes to these effects is unclear. Food intake, expression of thermogenic BAT proteins, and WAT lipolysis were measured after central or peripheral administration of Exendin-4 (EX4), a GLP1R agonist, to mice under intermittent-short exposure to CAF diet (3 h/d for 8 days) or a longer-continuous exposure to CAF diet (24 h/d for 15 days). Ex-vivo lipolysis was measured after EX4 exposure to WAT samples from mice fed CAF or control diet for 12 weeks. . During intermittent-short exposure to CAF diet (3 h/d for 8 days), third ventricle injection (ICV) and intra-peritoneal administration of EX4 reduced palatable food intake. Yet, during a longer-continuous exposure to CAF diet (24 h/d for 15 days), only ICV EX4 administration reduced food intake and body weight. However, this exposure to CAF diet blocked the increase in uncoupling protein 1 (UCP1) caused by ICV EX4 administration in mice fed control diet. Finally, GLP1R expression in WAT was minimal, and EX4 failed to increase lipolysis ex-vivo in WAT tissue samples from mice fed CAF or control diet for 12 weeks. . Exposure to a CAF diet during the early stages of obesity reduces the effects of peripheral and central GLP1R agonists, and WAT does not express a functional GLP1 receptor. These data support that exposure to the obesogenic food environment, without the development or manifestation of obesity, can alter the response to GLP1R agonists. .

Paraoxonase-1: How a xenobiotic detoxifying enzyme has become an actor in the pathophysiology of infectious diseases and cancer

Both infectious and non-infectious diseases can share common molecular mechanisms, including oxidative stress and inflammation. External factors, such as bacterial or viral infections, excessive calorie intake, inadequate nutrients, or environmental factors, can cause metabolic disorders, resulting in an imbalance between free radical production and natural antioxidant systems. These factors may lead to the production of free radicals that can oxidize lipids, proteins, and nucleic acids, causing metabolic alterations that influence the pathogenesis of the disease. The relationship between oxidation and inflammation is crucial, as they both contribute to the development of cellular pathology. Paraoxonase 1 (PON1) is a vital enzyme in regulating these processes. PON1 is an enzyme that is bound to high-density lipoproteins and protects the organism against oxidative stress and toxic substances. It breaks down lipid peroxides in lipoproteins and cells, enhances the protection of high-density lipoproteins against different infectious agents, and is a critical component of the innate immune system. Impaired PON1 function can affect cellular homeostasis pathways and cause metabolically driven chronic inflammatory states. Therefore, understanding these relationships can help to improve treatments and identify new therapeutic targets. This review also examines the advantages and disadvantages of measuring serum PON1 levels in clinical settings, providing insight into the potential clinical use of this enzyme.

Ultra-Processed Food Intake Is Associated with Non-Alcoholic Fatty Liver Disease in Adults: A Systematic Review and Meta-Analysis.

Non-alcoholic fatty liver disease (NAFLD) is associated with overweight/obesity, metabolic syndrome and type 2 diabetes (T2D) due to chronic caloric excess and physical inactivity. Previous meta-analyses have confirmed associations between ultra-processed food (UPF) intake and obesity and T2D. We aim to ascertain the contribution of UPF consumption to the risk of developing NAFLD. We performed a systematic review and meta-analysis (PROSPERO (CRD42022368763)). All records registered on Ovid Medline and Web of Science were searched from inception until December 2022. Studies that assessed UPF consumption in adults, determined according to the NOVA food classification system, and that reported NAFLD determined by surrogate (steatosis) scores, imaging or liver biopsy were included. The association between UPF consumption and NAFLD was assessed using random-effects meta-analysis methods. Study quality was assessed, and evidence credibility evaluated, using the Newcastle Ottawa Scale and NutriGrade systems, respectively. A total of 5454 records were screened, and 112 records underwent full text review. From these, 9 studies (3 cross-sectional, 3 case-control and 3 cohort), analysing 60,961 individuals, were included in the current review. Both moderate (vs. low) (pooled relative risk 1.03 (1.00-1.07) (p = 0.04) (I2 = 0%)) and high (vs. low) (1.42 (1.16-1.75) (<0.01) (I2 = 89%)) intake of UPF significantly increased the risk of NAFLD. Funnel plots demonstrate low risk of publication bias. Consumption of UPF is associated with NAFLD with a dose-response effect. Public health measures to reduce overconsumption of UPF are imperative to reduce the burden of NAFLD, and the related conditions, obesity and T2D.

From a toxin to an obesogen: a review of potential obesogenic roles of acrylamide with a mechanistic approach.

Obesity and obesity-related disorders such as cancer, type 2 diabetes, and fatty liver have become a global health problem. It is well known that the primary cause of obesity is positive energy balance. In addition, obesity is the consequence of complex gene and environment interactions that result in excess calorie intake being stored as fat. However, it has been revealed that there are other factors contributing to the worsening of obesity. The presence of nontraditional risk factors, such as environmental endocrine-disrupting chemicals, has recently been associated with obesity and comorbidities caused by obesity. The aim of this review was to examine the evidence and potential mechanisms for acrylamide having endocrine-disrupting properties contributing to obesity and obesity-related comorbidities. Recent studies have suggested that exposure to environmental endocrine-disrupting obesogens may be a risk factor contributing to the current obesity epidemic, and that one of these obesogens is acrylamide, an environmental and industrial compound produced by food processing, particularly the processing of foods such as potato chips, and coffee. In addition to the known harmful effects of acrylamide in humans and experimental animals, such as neurotoxicity, genotoxicity, and carcinogenicity, acrylamide also has an obesogenic effect. It has been shown in the literature to a limited extent that acrylamide may disrupt energy metabolism, lipid metabolism, adipogenesis, adipocyte differentiation, and various signaling pathways, and may exacerbate the disturbances in metabolic and biochemical parameters observed as a result of obesity. Acrylamide exerts its main potential obesogenic effects through body weight increase, worsening of the levels of obesity-related blood biomarkers, and induction of adipocyte differentiation and adipogenesis. Additional mechanisms may be discovered. Further experimental studies and prospective cohorts are needed, both to supplement existing knowledge about acrylamide and its effects, and to clarify its established relationship with obesity and its comorbidities.

Processed foods, socio-economic status, and peri-urban obesity in India

The ‘State of Food Security and Nutrition in the World 2020′ report states that switching to healthy diets will both prevent backsliding into hunger and help countries meet their sustainability goals. In 2019–2020, 17 percent of India’s adult population was undernourished. At the same time, however, 23 percent of all adults were obese. The increasing prevalence of obesity implies that improving diets and reducing risks for obesity and non-communicable diseases (NCDs) is a major food security challenge for India in the coming years. Overconsumption of calories from processed foods is known to increase the risk of obesity. To gain insights into the dietary transition and its relationship with obesity, we use cross-sectional data from a primary socio-economic survey conducted in the rural-urban interface of Bangalore, a mega-city in India that is characterized by high economic development. We show that for women in lower-middle socio-economic status (SES) groups, higher share of calories from semi-processed foods (SPF) is associated with a higher prevalence of obesity, while excess consumption of calories from ultra-processed foods (UPF) is associated with a higher obesity prevalence among women in higher SES groups. Older women and women who consume above the recommended daily allowance (RDA) of calories are more vulnerable to excess calories from SPF consumption than younger women and women who consume less than the RDA of calories. Furthermore, a lower prevalence of obesity is observed among women who consume excess calories from SPF but engage in labor-intensive occupational activity. These results speak to the need for interventions that incentivize weight loss and increased physical activity. The result that SPF consumption is associated with an increased prevalence of obesity especially among lower-middle SES group calls for interventions that increase access to and affordability of healthy diets. Policy instruments such as diversifying the public distribution system (PDS) are important to improve accessibility and affordability of healthy diets. In addition, increasing sugar and processed food taxes and incentivizing companies to invest in culturally sensitive food labeling should be considered to shift consumer demand towards healthier diet choices.

Inclusive diets within planetary boundaries

Inclusive diets within planetary boundaries

Abstract #1404927: Glycogenic Hepatopathy is a Rare Reversible Condition with Optimal Glycemic Control in Type 1 Diabetes Mellitus

Glycogenic hepatopathy (GH) is a rare complication of type 1 DM due to over-insulin use to achieve glycemic control due to excessive calorie intake. GH developed due to the accumulation of glycogen in hepatocytes predominantly seen in the pediatric population with poorly controlled DM type 1 and rarely seen in DM 2 and characterized by transient transaminitis and hepatomegaly. Liver biopsy is the gold standard and non-invasive tests are having a limited role. 18-year-old Hispanic male with poorly controlled type 1 DM, dyslipidemia, and post-ablative hypothyroidism. The patient was non-compliant with medical treatment leading to multiple hospitalizations for diabetes ketoacidosis (DKA) and also hypoglycemic events. The patient was clinically asymptomatic (denied any nausea/vomiting or abdominal pain) and was never been diagnosed with liver dysfunction in the past. Physical examination was significant for the enlarged liver but no splenomegaly, otherwise unremarkable. Initial routine labs revealed elevated aminotransferases ALT 1329 IU/L and AST 1987 IU/L otherwise CBC and CMP, TSH were unremarkable. HbA1c was 13.7. A liver ultrasound revealed diffuse fatty infiltration and hepatomegaly (20.5 cm). No signs of biliary stones or obstruction. Serology for viral Hepatitis A’’, ‘B’ and ‘C’ were negative. Autoimmune hepatitis workup (ANA, ASMA, AMA) and celiac serology were negative. The patient underwent a liver biopsy and showed diffuse hepatocyte swelling with frequent glycogenated nuclei consistent with glycogenic hepatopathy with minimal inflammation and no evidence of steatosis. Minimal sub-sinusoidal fibrosis (Fibrosis stage 0/6). The patient was counseled for strict glycemic control with a low-carb diet (portion control) and proper use of insulin with close office follow-up and regular monitoring of blood sugar at home. Within 6 months, HbA1C improved from 13.7% to 9.8% and ALT improved from 1329 to 51 IU/L and AST decreased from 1987 to 57 IU/L. During a nine-month follow-up visit, AST and ALT remained low at 44 and 31 IU/L respectively. Patient followed the The patient underwent a repeat liver biopsy which revealed minimal accumulation of glycogen deposits and minimal hepatocyte inflammation and no evidence of fibrosis. GH and NAFLD are indistinguishable clinically and NAFLD is more prevalent in DM although GH is a revertible disease within 2-14 weeks with better glycemic control. The pathophysiology of GH is incompletely understood. It is believed to be the consequence of recurrent fluctuations of glucose level with hyperglycemia and hypoglycemia and hyperinsulinism. Supra-physiological doses of insulin to manage blood sugar are believed to be the cause of this condition. Awareness of Glycogenic hepatopathy is essential, and the proper management of elevated liver enzymes is to be addressed in uncontrolled type 1 DM patients. Recurrence of GH has been reported with repeated episodes of DKA. Further research is needed to investigate this phenomenon.

Obesity and Impact On Thyroid Hormone and Subclinical Hypothyroidism

Background: Obesity is a metabolic disorder due to physical inactivity associated with increased consumption of calories. The excess calorie is stored as fat in adipose tissue, the fat loaded adipose tissue stimulates inflammatory pathway. The secreted inflammatory cytokines influence the sodium iodide transporter on the surface of thyroid gland. It causes decreased Thyroid hormone (TH) secretion &amp; elevated Thyroid Stimulation Hormone (TSH). the energy metabolism of the body is regulated by TH, decreased TH secretion in obesity disturbs energy metabolism. Material &amp; Methods: The study population are the patients attending OPD of medicine a tertiary hospital in Bhopal, Madhya Pradesh (Central India). Total 25 patients are selected for the study based on their anthropometric measurements (Weight, Height, BMI) confirmed them as obese. Of them 16 are males and 9 are females aged &gt;35 years and are compared with equal number of age matched control population. Results: The values obtained after investigation of various parameters of study as well as control is analysed using SPSS software. The obtained mean, SD values of these parameters are as follows. Conclusion: The obesity due to excessive calorie intake with low physical activity deposits more fat into adipose tissue. The fat loaded adipocytes not only increases blood lipids but also aggravates inflammatory pathways. The secreted inflammatory cytokines (IL-1, 12,18, TNF- α , IFN influences thyroid function by a change in lodide transport across the thyroid gland.

Feeding with resistant maltodextrin suppresses excessive calorie intake in a high-fat diet, mediated by changes in mouse gut microbiota composition, appetite-related gut hormone secretion, and neuropeptide transcriptional levels

Consuming resistant maltodextrin (RMD) decreases food intake and increase appetite-related gut hormones, but the underlying mechanisms have remained unknown. Therefore, we aimed to elucidate the mechanisms underlying the effects of RMD feeding on food intake (appetite) using Institute of Cancer Research male mice fed with a high-fat diet (HFD-cellulose group) or HFD in which cellulose was replaced with RMD (HFD-RMD group). Feeding mice with an HFD-RMD for approximately 8 weeks inhibited excessive calorie intake and altered the gut microbiota composition. Excessive calorie intake was inhibited for several days in mice fed only with an HFD-cellulose and transplanted with fecal microbiota from the HFD-RMD group (FMT-HFD-RMD group). Moreover, in the HFD-RMD and FMT-HFD-RMD groups, serum active glucagon-like peptide (GLP)-1 and peptide tyrosine tyrosine (PYY) levels were significantly higher, and appetite-related neuropeptide gene transcription in the hypothalamus were significantly altered, compared with the HFD-cellulose and FMT-HFD-cellulose groups. These results suggested that the long-term RMD intake changed the gut microbiota composition, increased the GLP-1 and PYY secretion, and altered the appetite-related neuropeptide gene transcription in the hypothalamus, leading to suppressed excessive calorie intake in an HFD.

Habitual daily intake of a sweet and fatty snack modulates reward processing in humans

Western diets rich in fat and sugar promote excess calorie intake and weight gain; however, the underlying mechanisms are unclear. Despite a well-documented association between obesity and altered brain dopamine function, it remains elusive whether these alterations are (1) pre-existing, increasing the individual susceptibility to weight gain, (2) secondary to obesity, or (3) directly attributable to repeated exposure to western diet. To close this gap, we performed a randomized, controlled study (NCT05574660) with normal-weight participants exposed to a high-fat/high-sugar snack or a low-fat/low-sugar snack for 8weeks in addition to their regular diet. The high-fat/high-sugar intervention decreased the preference for low-fat food while increasing brain response to food and associative learning independent of food cues or reward. These alterations were independent of changes in body weight and metabolic parameters, indicating a direct effect of high-fat, high-sugar foods on neurobehavioral adaptations that may increase the risk for overeating and weight gain.

Nutrient support for preschool children with psychomotor disorders

Background. Children with psychomotor disorders are vulnerable to nutrient deficiencies, which significantly complicate their rehabilitation. The purpose of our study was to identify the nutrient deficiencies in preschool children with psychomotor disorders by analyzing their diet, revealing the relationship between the detected nutrient deficiencies, the gender of the children and their psychomotor disorders in order to improve the effectiveness of rehabilitation. Materials and methods. The diet of 53 preschool children with psychomotor disorders was analyzed using the Child’s Eating Behavior questionnaire, followed by analysis with the licensed computer program Dietplan7. Statistical processing was conducted using parametric and correlational analysis. Results. Different violations of eating behavior in children with psychomotor disorders were determined. They included, in particular, the refusal to consume a number of healthy foods, while preferring mainly semi-finished products, fast food, smoked products, rich in salt and sugar, spices. The diet of most examined children was unbalanced in terms of the content of basic nutrients, vitamins and minerals: an excess of proteins, fats and calories, numerous combined vitamin and mineral deficiencies were detected. A reliable correlation was found between the daily consumption of nutrients and neurological pathology that was most significant in subgroups of children with mental retardation. Conclusions. In the food diet of many children with psychomotor disorders, there were unhealthy eating patterns typical of the Western diet. Numerous deficiencies in the daily consumption of basic nutrients, including vitamins and minerals, were found in them, which had a probable correlation with neurological disorders. To improve the effectiveness of the rehabilitation of children with psychomotor disorders, a multidisciplinary approach is advisable with the involvement of a nutritionist for personalized correction of the child’s diet.

Adipose-targeted SWELL1 deletion exacerbates obesity- and age-related nonalcoholic fatty liver disease.

Healthy expansion of adipose tissue is critical for the maintenance of metabolic health, providing an optimized reservoir for energy storage in the form of triacylglycerol-rich lipoproteins. Dysfunctional adipocytes that are unable to efficiently store lipid can result in lipodystrophy and contribute to nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome. Leucine-rich repeat containing protein 8a/SWELL1 functionally encodes the volume-regulated anion channel complex in adipocytes, is induced in early obesity, and is required for normal adipocyte expansion during high-fat feeding. Adipose-specific SWELL1 ablation (Adipo KO) leads to insulin resistance and hyperglycemia during caloric excess, both of which are associated with NAFLD. Here, we show that Adipo-KO mice exhibited impaired adipose depot expansion and excess lipolysis when raised on a variety of high-fat diets, resulting in increased diacylglycerides and hepatic steatosis, thereby driving liver injury. Liver lipidomic analysis revealed increases in oleic acid-containing hepatic triacylglycerides and injurious hepatic diacylglyceride species, with reductions in hepatocyte-protective phospholipids and antiinflammatory free fatty acids. Aged Adipo-KO mice developed hepatic steatosis on a regular chow diet, and Adipo-KO male mice developed spontaneous, aggressive hepatocellular carcinomas (HCCs). These data highlight the importance of adipocyte SWELL1 for healthy adipocyte expansion to protect against NAFLD and HCC in the setting of overnutrition and with aging.

You are what you eat? Rodent study suggests defended body weight mainly dictated by fatcontent of diet.

Preclinical and clinical data suggest that body weight (i.e., body fat) is physiologically regulated, and the high heritability seen from monozygotic twin studies suggests a genetic basis to one's defended body weight. Genome-wide association studies have found that a high proportion of variants that correlate with elevated body mass index are expressed in the central nervous system, signifying that the molecular predicates that likely encode for defended body weight will be found in the brain [(1)]. In this context, an individual integrates peripheral signals (e.g., adipokines, myokines, hepatokines) relaying the metabolic state of various tissues to the brain and reacts to maintain relatively stable weight. However, the recent increased prevalence of obesity/overweight reveals that environmental factors must be influencing this system, and why some people are more susceptible to weight gain in a given environment is not fully understood [(2)]. In this issue, Fang et al. [(3)] present an interesting and thorough set of experiments that demonstrate how fat content in diet affects defended body weight in C57BL/6N mice. By changing the macronutrient composition (fat and carbohydrate) of diets and undertaking switches in diet at different ages (young and adult) and for different durations (4, 8, or 24 weeks), as well as putting mice through rounds of weight gain and weight loss (yo-yo dieting), they provide strong evidence that the major driver of defended body weight in these animals is the amount of fat within the diet. The key takeaway message is that higher-fat diets (HFDs, i.e., diets with 45% fat or more) cause defense of an elevated body weight plateau, whereas lower-fat diets (LFDs, i.e., diets with 10% or 25% fat) cause defense of a lower body weight plateau irrespective of the age at which the diets start or their duration. Furthermore, HFD- and LFD-fed animals showed similar physiology to a 16-hour fast, and switching mice back to LFDs after HFD feeding caused rapid and sustained weight loss, with most groups returning to the LFD-fed weight. They suggest that HFDs do not impede normal physiological defense of body weight but rather cause an increase to a new defended body weight. This paradigm shift is subtle but important. Although understanding the mechanisms behind these findings is beyond the scope of the paper, increases in circulating lipids from diets have been causally linked to inflammation of the hypothalamus and may, in part, explain the present findings [(4)]. Of course, humans are exposed to many different variables that are hard to replicate in rodent models. For example, workers are much more sedentary than in the past, numerous excess calories are consumed through simple sugars found in soft drinks, and we undertake numerous activities and hobbies that directly affect our daily metabolic rate. All of these parameters likely contribute to our defended body weight; however, the diet likely remains one of the major modifiable inputs. The search for the molecular underpinnings of defense of body weight will continue to evolve with each new study adding to our overall understanding of this important physiological regulation; however, this study [(3)] clearly demonstrates that fat content seems directly implicated in body weight regulation. The type of food we eat likely influences the system of how our body weight is regulated, and understanding these interactions is crucial. This study suggests that eating diets high in fat may result in the overconsumption of calories leading to elevated body weight. Would you like meringue and gruyère double cream just after having eaten a large fondue? Of course you would. Open access funding provided by Universite de Fribourg. The author declared no conflict of interest.

Gender differences in the risk of developing obesity related disease can be explained by sex‐specific molecular signatures that regulates adipose endothelial cell growth

Obesity is the excessive growth of adipose tissue resulting from the chronic consumption of excess calories and is a recognised risk factor for developing cardio-metabolic diseases. There is however a significant variation in the size and expandibility of different adipose tissue in humans. The inability of adipose tissue to expand “safely” leads to ectopic fat deposition, causing insulin resistance, type 2 diabetes and cardiovascular conditions – which are more prevalent in men than women. Thus, the mechanisms that control the expandability of adipose tissue are key factors in determining diabetes risk in obesity. An interesting study from York University have provided new insights on the biological underpinning in gender differences in the risk of developing obesity-related diseases. Previous study from this group has observed that when mice become obese, females grow more new blood vessels to supply the expanding fat tissue with oxygen and nutrients, whereas males grow a lot less. To understand the mechanism regulating this, the team used software to help sift through thousands of genes to zero in on the ones that would be associated with blood vessel growth. They discovered that processes associated with the proliferation of new blood vessels were high in the female mice, whereas the males had a high level of processes associated with inflammation. Thereafter, the investigators examined the behaviour of the endothelial cells ex-vivo. Interestingly, they observed that even when these cells were studied ex-vivo, male and female endothelial cells still behave very differently from each other - female endothelial cells replicated faster, while male endothelial cells displayed greater sensitivity to an inflammatory stimulus. Further studies to investigate the effects of specific genes in humans that regulate endothelial cells growth will provide potential therapeutic target to manage and treat obesity related cardio-metabolic diseases. The study was funded by a grant through the Canadian Institutes of Health Research, as well as the Natural Science and Engineering Research Council of Canada and York's Faculty of Health.

Cellular Senescence In White Adipose Tissue of Obese Mice

Obesity is defined as excessive fat accumulation that presents as risk factor for various chronic diseases such as diabetes, cardiovascular disease, hypertension, hyperlipidemia, and cancer. The number of obese population has reached 1 trillion people worldwide and is expected to increase at 42% of the world population until 2030. Excess calories in obesity increase the formation of Reactive Oxygen Species (ROS) that cause DNA damage. DNA damage results in inhibition of the cell cycle and lead to cellular senescence. The mechanism of cell senescence caused by cell cycle inhibition can occur through the cellular senescence pathway by p53/p21 WAF1/CIP1 and p16INK4A / pRB. White adipose tissue is an appropriate reservoir to study of cellular senescence. White adipose tissue of obese model mice showed that there was cellular senescence with marked increase in p21 and p16 gene expression in obese mice

Long-term consumption of fermented pork fat-based diets differing in calorie, fat content, and fatty acid levels mediates oxidative stress, inflammation, redox imbalance, germ cell apoptosis, disruption of steroidogenesis, and testicular dysfunction in Wistar rats.

There is a dearth of experimental evidence available as to whether the consumption of fermented pork fat (FPF) food has any harmful effects on metabolism and reproduction due to its excessive calories, high fat content, and fatty acid methyl ester (FAME) levels. We hypothesized that exposure to a FPF-diet with excessive calories, a high fat content, and high FAME levels alters testicular physiology and metabolism, leading to permanent damage to the testicular system and its function. Thirteen-week-old male rats (n = 20) were assigned to a high-calorie, high-fat diet (FPF-H, fat-60%, 23kJ/g), a moderate-calorie, moderate-fat diet (FPF-M, fat-30%, 17.5kJ/g), a low-calorie and low-fat diet (FPF-L, fat-15%, 14.21kJ/g) compared to the standard diet (Control, fat-11%, 12.56kJ/g) orally for 90days. GC-MS analysis of the three FPF-diets showed high quantities of saturated fatty acids (SFAs) and polyunsaturated fatty acids-ω6 (PUFA-ω6) and low levels of monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids-ω3 (PUFA-ω3) compared to the control diet. Consequently, the levels of serum FAMEs of the FPF-diet fed rats were significantly increased. In addition, a high level of n-6:n-3 PUFA towards PUFA-ω6 was observed in the serum of FPF-diet fed rats due to the high content of linoleic, γ-linolenic, and arachidonic acid. Long-term consumption of FPF-diets disturbed the anthropometrical, nutritional, physiological, and metabolic profiles. Furthermore, administration of FPF-diets generated metabolic syndrome (dyslipidemia, leptinemia, insulin resistance, obesity, hepato-renal disorder and function), increased the cardiovascular risk factors, and triggered serum and testis inflammatory markers (interleukin-1↑, interleukin-6↑, interleukin-10↓, leukotriene B4↑, prostaglandin↑, nitric oxide↑, myeloperoxidase↑, lactate dehydrogenase↑, and tumor necrosis factor-α↑). Activated testis oxidative stress (conjugated dienes↑, lipid hydroperoxides↑, malondialdehyde↑, protein carbonyl↑, and fragmented DNA↑) and depleted antioxidant reserve (catalase↓, superoxide dismutase↓, glutathione S-transferase↓, reduced glutathione↓, glutathione disulfide↑, and GSH:GSSG ratio↓) were observed in FPF-diet fed rats. Disrupted testis histoarchitecture, progressive deterioration of spermatogenesis, poor sperm quality and functional indices, significant alterations in the reproductive hormones (serum and testis testosterone↓, serum estradiol↑, serum luteinizing hormone↓, and follicle-stimulating hormone↑), were noted in rats fed with FPF diets than in the control diet. Severe steroidogenic impairment (steroidogenic acute regulatory protein, StAR↓; 3β-hydroxysteroid dehydrogenase, 3β-HSD↓; and luteinizing hormone receptor, LHR↓), deficiency in germ cells proliferation (proliferating cell nuclear antigen, PCNA↓), and abnormally enhanced testicular germ cell apoptosis (terminal deoxynucleotidyl transferase dUTP nick end labeling, TUNEL assay↑; B-cell lymphoma-2, BCL-2↓; Bcl-2-associated X protein, BAX↑; and BAX/BCL-2 ratio↑) were remarked in the FPF-diet administered rats in comparison with the control diet. In conclusion, the long-term feeding of an FPF-diet with excessive calories, a high fat content, and high FAME levels induced oxidative stress, inflammation, and apoptosis, resulting in metabolic syndrome and hampering male reproductive system and functions. Therefore, the adoption of FPF diets correlates with irreversible changes in testis metabolism, steroidogenesis, germ cell proliferation, and apoptosis, which are related to permanent damage to the testicular system and function later in life.

Impact of Starch Gelatinization on Digestibility and Human Health

AbstractThe availability of digestible energy from consumed starch depends on whether the starch is in an amorphous/digestible or ordered/less digestible form. The capacity of man to digest starch has been an evolutionary process where early hunter gatherers would have eaten crops with relatively low amounts of starch that is also not cooked. This requires a lot of digestive effort to extract calories and hence the efficiency in the body of the starch digestive process. Modern man, however, cooks (and has done for centuries) starchy crops. This, combined with the high starch contents of foods that are also readily available, has led to excess calories in the diet (from other nutrient sources too) and associated disease states. This article is designed to set the gelatinization of starch in the context of health and how starch processing needs to be regulated to control excess calories in the diet – many from starch. Key messages to gain from this review are that i) starch is a potential source of energy and depending on how and when it is processed and consumed it will impact on energy and health plus that ii) overall management of calories – including from digestible starch – is critical for optimal health.

Investigating the Impact of Food Rewards on Children’s Motivation to Participate in Sport

Children who are physically active and involved in organized sport report having the unhealthiest diets. Research suggests excessive calories may be attributed to the prevalence of fast food and candy which are often provided as rewards in sport. This study explored the use of food as a reward in youth sport and the perceived impact it has on children's motivation to participate in recreational soccer and ice hockey. A multiple instrumental case study approach was utilized. Children aged 4-12 (n = 64), parents (n = 30), and coaches (n = 18) were recruited within central and northeastern Ontario, Canada to participate in focus groups and individual interviews. Transcribed audio recordings underwent inductive thematic analysis. Key themes included: Fun and fast: The culture of food in youth soccer and hockey; (Un)importance of food rewards: The how and why of motivating children in sport; and Youth sport is expensive: Gratitude for sponsorship in youth sport. Themes explain the role of food and food rewards as an element of the youth sport culture as well as the importance of sponsors, regardless of food affiliation, in youth sport. Overall, children's participation and effort would continue without food rewards; however, they continue to be offered food to motivate and celebrate performance in youth sport. Findings highlight the need to increase knowledge and awareness among parents and coaches on what truly motivates children to help foster healthier strategies for celebrating success and supporting lifelong physical activity.

The relationship between physical activity and diabetes in middle-aged and elderly people.

To investigate the association between diabetes symptoms and physical activity (PA) levels among middle-aged and older Chinese adults. Data for this study were obtained from 2018 Charles data. Z test, logistic regression analysis, and linear hierarchical regression analysis were performed in 5352 individuals aged ≥50 years with complete information. In terms of diabetes, 6.8% of the middle-aged and elderly people with diabetes were detected, and 93.2% of the middle-aged and elderly people without diabetes symptoms. The proportion of middle-aged and elderly people with high PA levels was 50.5%, and the proportion of middle-aged and elderly people with low PA was 49.5%. There was a significant positive correlation between low PA and diabetes (P < .05). After adjusting demographic characteristics (gender, registered permanent residence type, education level, age, widowhood) and health status characteristics (poor mood, asthma, hyperlipidemia, disability, memory disease, self-assessment of health status, hypertension, smoking, stroke, depression), there was still a statistical significance between PA level and diabetes (P < .05). The risk of diabetes of middle-aged and elderly people in China increases with age, while the risk of diabetes of middle-aged and elderly people with low level of PA is higher. The risk of diabetes is high among middle-aged and elderly people who are old, have poor self-evaluation health, suffer from hyperlipidemia, memory disease, and asthma. The middle-aged and old people should increase their PA levels to prevent and improve diabetes.