1,721,053 research outputs found
The hypothalamus and energy balance
No full textIn recent years the growing number of molecules implicated in energy homeostasis has raised nearly limitless possibilities for how body-weight regulation might occur. To better understand how energy homeostasis can be achieved, we describe the roles of individual hormonal and neuropeptide signalling pathways in the control of food intake and the means by which obesity can arise from defects in their function. The hypothalamus links the sensing of nutrients to the control of metabolism and feeding behaviour. Disruptions in the mechanisms of central nervous system (CNS) nutrient-sensing alter these homeostatic responses and contribute to the pathophysiology of obesity and type 2 diabetes mellitus. Experimental and epidemiological studies suggest that sleep loss may also play a role in the increased prevalence of diabetes and obesity. The molecular components of the circadian clock are present in the anterior hypothalamus. It is not therefore surprising that there is a close link between sleep and energy metabolism. In this review we also focus on physical exercise as a mechanism to restore physiological rhythm preventing hyperphagia and obesity in humans. Given its ability to reduce cerebral energy demands and therefore promote sleep, physical exercise could be beneficial for maintaining brain function and improving brain plasticity
Nutrients and whole-body energy metabolism: the impact of physical exercise
No full textFood is required as a fuel for the maintenance of energy-requiring processes that sustain life. Energy is needed to preserve the physicochemical environment of the body (homeostasis) and to sustain the organism’s activities. Although there are large inter-individual differences in energy requirements, much of the variance can be ascribed to fat-free mass, age, sex, and amount of physical activity. Genetic factors also appear to play an important role (see Chapters 1 and 4) [1]
Different postprandial plasma ghrelin responses elicited by intake of 6 commercial snack foods in healthy subjects
No full textSnacking is controversially discussed as a good habit in a healthy nutritional regimen. Obviously snack foods may be very different in determining glycemic and hormonal responses related to appetite and satiety. Serving-size, composition, macronutrients are only some of the factors that could trigger a wide hormonal cascade and therefore causing potential deleterious effects on metabolism. In the last decade there has been a great deal of interest to consider ghrelin as a potential target for treating obesity. It has been previously shown that rodents vaccinated against endogenous ghrelin could slow weight gain by decreasing feed efficiency, thus suggesting a primary role played by this hormone in energy homeostasis. Here, 20 healthy individuals (10M/10F; BMI 23.3±1.6; 35±6 yrs) underwent to OGTT (50-g) and 6 isoglucidic test-meal loads to assess glycemic index (GI), plasma insulin and ghrelin circulating levels induced by 6 commercial snack foods. Ghrelin was significantly lower 3 hours after the snack intake with respect to the basal condition in half of the snack foods (hazelnut chocolate: P<0.001; sponge cake2: P<0.001; chilled cake: P=0.02), whereas no differences were detected in plasma insulin and GI among all snack foods. If ghrelin could be meant as a crucial biomarker of satiation, those 3 snacks drove a nutritional status more propending for a long-lasting hunger-free period.
Our results indicate that snack foods are diverse in inducing plasma ghrelin levels under equivalent metabolic conditions. Further studies are needed to elucidate the role of ghrelin as hunger-hormone in the regulation of energy balance
Lipodystrophy HIV-related and FGF21: A new marker to follow the progression of lipodystrophy?
Full text linkRecently new evidence about fibroblast growth factor 21 (FGF21) highlights the opportunities to use this molecule in new pharmaceutical formulations to combat type 2 diabetes and metabolic syndrome. It is well known that HIV is per se a condition of insulin resistance and in particular the patient with HIV-related lipodystrophy has a condition strictly related to metabolic syndrome. Lipodystrophy is associated with severe metabolic side effects, including dyslipidemia, hepatic insulin resistance, and lipid oxidation impairment. Research carried out showed that FGF21 levels were significantly increased in untreated HIV-1-infected patients and the increase was much marked in HIV-1-infected antiretroviral-treated patients that have developed lipodystrophy and in the patients with greatest metabolic alterations. FGF21 is expressed mainly by the liver, but also by other tissues such as the thymus, adipose tissue, and skeletal muscle. Therefore, many researchers have considered the investigation of possible variations of FGF21 in patients with significant alterations in body composition both in regard to fat mass and lean mass. In the light of the possible interactions between FGF21 and metabolic syndrome, it seems interesting to evaluate the implication of this hormone in patients with HIV-related lipodystrophy who have a severe metabolic picture of insulin resistance with important alterations in body composition
Antropometry in HIV patients: effects of recombinant human growth hormone
No full textAbstract Patients with HIV infection treated with protease inhibitors (PIs) drugs for a long period have a prolonged life expectancy and an improvement of quality of life. Often, HIV-patients on PIs
develop a syndrome characterized by peripheral lipoatrophy, truncal fat accumulation, hyperlipemia and insulin resistance. In HIV-1 patients undergoing antiretroviral treatment, lipodystrophy is associated with peripheral fat wasting and central adiposity, dyslipidemia, insulin resistance, and increased intramuscular fat accumulation.
In HIV lipodystrophy fat distribution changes are heterogeneous and can include reduced subcutaneous fat and increased visceral fat. In literature there are evidences showing overnight growth
hormone (GH) secretion and pulse amplitude reduction in patients with HIV lipodystrophy, in response to standard GH stimulation test. Excess accumulation of visceral fat with increasing of intra-abdominal adiposity (central obesity) is also a typical feature of patients with GH deficiency. Recombinant human growth hormone (rhGH) can be a useful treatment to diminish excess visceral fat. Up to day there are evidences that GH therapy in HIV-infected patients with syndromes of central fat accumulation show a significant decrease of body fat. In this chapter, we discuss the anthropometry of lipodystrophy in HIV patients and the indication of rhGH treatment in HIV-related lipodystrophy
Recombinant human growth hormone : rationale for use in the treatment of HIV-associated lipodystrophy
No full textThe role of hormonal and metabolic alterations in HIV-associated lipodystrophy syndrome is not yet clear. In patients with HIV-1 undergoing antiretroviral treatment, lipodystrophy is associated with peripheral fat wasting and central adiposity, dyslipidemia, insulin resistance, and increased intramuscular fat accumulation. In HIV lipodystrophy, changes in fat distribution are heterogeneous and can include reduced subcutaneous fat as well as increased visceral fat. In the literature, there is evidence showing that overnight growth hormone (GH) secretion and pulse amplitude decrease in patients with HIV lipodystrophy, with rates of response to standardized GH stimulation being abnormal in at least 20% of these patients. Excess accumulation of visceral fat, central obesity, and increased intra-abdominal adiposity are also typical features of patients with GH deficiency. Recombinant human GH (rhGH) is a potential treatment to diminish excess visceral fat. Our group recently demonstrated that GH therapy in HIV-infected patients with syndromes of fat accumulation produced a significant decrease in body fat and a gain in lean tissue. In this article, we discuss the origin of lipodystrophy in HIV patients, and the use of rhGH treatment (benefits and adverse effects) in HIV-related lipodystrophy
Plasma Citrulline : a New Marker of Gut Epithelium Alteration in Obese Patients?
Full text linkObjectives: In the last decade gut microbial diversity was associated with the pathogenesis of obesity
in humans. Plasma citrulline was a simple and accurate biomarker for the severity of intestinal
failure and was associated with short bowel syndrome and alteration of gut permeability, being
developed as an alternative to D-xylose tolerance test for the diagnosis of an abnormal small
intestinal absorption of nutrients. This study was performed to ascertain whether obesity might
be associated with dysregulation of epithelial gut function. Methods: Fifteen obese individuals (5
M/10 F; BMI 37.4 ± 6.1 Kg/m2; 42 ± 6 yrs) and 15 healthy gender- and age-matched controls (6
M/9 F BMI: 22.7 ± 2.1 Kg/m2; 39 ± 7 yrs) underwent D-xylose load (25 g) and plasma citrulline,
plasma insulin, glucose and lipid profile testing. Results: Plasma citrulline was significantly lower
in the obese group (p = 0.045) with respect to controls, whilst total cholesterol, LDL and tryglicerides
concentration, insulin level and HOMA-IR were significantly higher in obese patients. In contrast,
after D-xylose load no difference in serum xylose was found between the two groups (p = ns).
Conclusions: Obese patients show a decreased citrulline concentration with respect to lean subjects.
Since citrulline is a known marker of intestinal health, alterations in the gut epithelium are likely
to be associated with the obesity syndrome. We propose to measure citrulline level in obese patients
on a routine basis
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