Womens health man vitaminas diabetas heart we. Doc. Eglė Varanauskienė KMU Endokrinologijos klinika - ppt download

App'en er din digitale adgang til. Doctoral student: A. The doctor can recommend the iron studies test if you exhibit certain symptoms like headaches, weakness, and fatigue, accelerated heartbeat, abdominal pain, joint pain, tiredness, and dizziness. The endogenous cannabinoid system affects energy balance via central orexigenic drive and peripheral lipogenesis.

Presentation on theme: "Doc. Even remote controls and mobile telephones deprive us of physical activity and can lead to the accumulation of almost a kilogram of adipose tissue every year.

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Furthermore, just one lump of extra sugar per day also leads to the accumulation of almost a kilogram of additional body fat over a year. It is this imbalance between energy intake and physical activity over time that results in body fat accumulation. However, taking a little more activity each day, for example by using the stairs instead of the escalator, would counterbalance this and maintain the balance in body weight.

Per 1 val. JAMA ; — The largest part of our energy expenditure comes from our resting energy requirement — the energy we need to keep our bodies alive. We normally refer to that as resting metabolic rate but we know that activity and thermogenesis are also factors involved in dissipating energy. One of the factors in the increasing prevalence and incidence of obesity seems to be declining activity levels. At the same time, the availability, palatability and affordability of food has never been greater and it is thus easy for people to womens health man vitaminas diabetas heart we consume.

The increasing prevalence of obesity is expected to continue for the foreseeable future. By it was estimated to be about million, and WHO predicts that the number will increase to at least million by the year JAV populiacija proc.

Duomenys gauti: World Health Organization.

Adapted from Smyth S et al. Nat Med. References: 1. Astrup A, Finer N. Redefining type 2 diabetes: 'diabesity' or 'obesity dependent diabetes mellitus'? Obes Rev. Smyth S, Heron A. Diabetes and obesity: The twin epidemic. In addition, the metabolic syndrome existed if any two of these components were present in a person with type 2 diabetes. The net result is a lowered risk of CHD-related events.

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Vigorous control of glycemia with insulin, metformin, and sulphonylureas clearly improves microvascular outcomes and may benefit macrovascular outcomes to some degree as well. Iškilūs pažeidimai Amžius m.

PDAY Circulation. Kartu slopinamas augimo hormono, Prolaktino, gonadotropinų — lytinių liaukų ašių aktyvumas. Gali padidėti kortizolio ir sumažėti augimo hormono, prolaktino kiekis kraujyje. Visuose nutukimo modeliuose, išskyrus POMC produkcijos defektą ir MC4 geno mutacijos modelį — kartu nustatoma rezistencija insulinui The adipocyte in insulin resistance: key molecules and the impact of the thiazolidinediones.

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Lašienė, L. Lašas, m. Fat deposits are present in the liver and muscle as well as the metabolically more active intra-abdominal fat. DeFronzo RA.

Br J Diabetes Vasc Dis. References Groop LC. Diabetes Obes Metab ; 1: S1—S7. DeFronzo R. Diabetes ; — Inzucchi SE. JAMA ; ; — Kahn SE. Am J Med ; 25— Stumvoll M. Lancet ; — Groop LC. Molecular pathogenesis of diabetes mellitus.

Doc. Eglė Varanauskienė KMU Endokrinologijos klinika

Karger; ; — Among these are alterations in the insulin resistance of hepatic and skeletal muscle, pancreatic beta-cell damage, nephropathy, retinopathy, neuropathy, and, in a large proportion of diabetic patients, CVD. These actions may cause more damage to the vascular wall than that due to hyperglycemia oxidative stress, glycation alone. According to the portal theory, high concentrations of FFA from intra-abdominal adiposity reach the liver via the portal vein, where they impair metabolic function.

Normally, the postprandial insulin rise suppresses lipolysis, but intra-abdominal adipocytes may be more insulin resistant than subcutaneous adipocytes. The excess portal FFA load induces hepatic insulin resistance, leading to increased hepatic glucose production and hyperinsulinaemia. The hypertriglyceridaemia induces increased secretion of triglyceride-rich VLDL-cholesterol, which is converted to LDL-cholesterol in the circulation, as lipolysis degrades its triglyceride content.

The relatively high original triglyceride content results in LDL particles that are smaller and denser than those present in an individual without intra-abdominal adiposity and insulin resistance. This results ultimately in small, dense HDL particles that are more rapidly catabolised.

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The net result is an overall reduction in HDL-cholesterol. FFA are also toxic to the β-cell at high concentrations, leading to long-term impairment of β-cell function and impaired insulin release. Mechanisms of the free fatty acid-induced increase in hepatic glucose production. Abdominal obesity and dyslipidemia in the metabolic syndrome: importance of type 2 diabetes and familial combined hyperlipidemia in coronary artery disease risk.

The metabolic syndrome. Pleiotropic effects of fatty acids on pancreatic beta-cells.

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J Cell Physiol ; Effects of free fatty acids on insulin secretion in obesity. Lam TK et al. Carr MC et al. J Cell Physiol ;; Zraika S et al. The direct adverse effects of intra-abdominal adiposity occur via the secretion of a range of bioactive substances.

These include: a Increased secretion of plasminogen activator inhibitor-1 PAI-1the endogenous inhibitor of tissue plasminogen activator tPA. Increased PAI-1 secretion increases the risk of an intravascular thrombus. Decreased secretion of adiponectin in the setting of intra-abdominal adiposity implies increased cardiovascular risk.

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Intravascular inflammation is a key early event in atherogenesis. Failure of fat cell proliferation, mitochondrial function kaip susirgti hipertenzija fat oxidation results in ectopic fat storage, insulin resistance and type II diabetes mellitus. Coppack SW. Pro-inflammatory cytokines and adipose tissue. Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor The analysis presented here was designed to define the association between waist circumference and the risk of developing type 2 diabetes.

The risk of developing type 2 diabetes increased linearly with an increasing waist circumference. The relative risk for women at the 90th percentile womens health man vitaminas diabetas heart we waist circumference equivalent to a womens health man vitaminas diabetas heart we measurement of 92 cm [36 in] was 5.

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High waist circumference is a powerful predictor of an increased risk of developing type 2 diabetes Wang Y et al, Am J Epidemiol. Body fat distribution and risk of non-insulin-dependent diabetes mellitus in women. The Nurses' Health Study.

Head — Prof. Docents: Dr. Ališauskas, Dr.

Am J Epidemiol ; Wang Y, et al. Comparison of abdominal adiposity and overall obesity in predicting risk of type 2 diabetes among men. Am J Clin Nutr. During 8 years of follow-up, there was a direct, independent and continuous relationship between waist circumference and age-adjusted risk of CHD. Abdominal adiposity and coronary heart disease in women. J Am Med Assoc ;—8. A population of 20, patients at high cardiovascular risk through the presence of coronary disease, other arterial disease or diabetes were randomly assigned to treatment with simvastatin or placebo for an average of 5 years.

Total cholesterol and Womens health man vitaminas diabetas heart we were markedly reduced by treatment with the statin mean changes from baseline of —1. However, other lipid components, such as triglycerides of HDL-C impact importantly on cardiovascular risk and were changed only slightly in the study womens health man vitaminas diabetas heart we changes from baseline of —0. We may need to look beyond effects on LDL-C to achieve greater results in the management of overall cardiovascular risk.

Lancet ; Intra-abdominal adiposity drives the progression of multiple risk factors directly, through the secretion of excess free fatty acids and inflammatory adipokines, and decreased secretion of adiponectin. The important contributions of IAA to dyslipidaemia and insulin resistance provide an indirect, though clinically important, link to the genesis and progression of atherosclerosis and cardiovascular disease.

The location of excess IAA is an important determinant of cardiometabolic risk. Elevated CRP is an indicator of inflammation.

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Abdominal obesity has been shown to be associated with the inflammation cascade, with adipose tissue expressing a number of inflammatory cytokines. Inflammation is now believed to play a role in the development of atherosclerosis and type 2 diabetes.

Elevated levels of CRP are considered to be predictive of cardiovascular disease and insulin resistance. Elevated FFA levels appear to play a significant role in the cause of insulin resistance.

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It has been suggested that elevated FFAs and intracellular lipids inhibit the insulin signaling mechanism, leading to decreased glucose transport to muscle. FFAs also play a mediating role between insulin resistance and β-cell dysfunction, indicating that a reduction in FFA level could be a desirable therapeutic target.

Adiponectin is an adipose tissue-specific circulating protein which is involved in the regulation of lipid and glucose metabolism. Adiponectin has been shown to be reduced in adults with obesity and type 2 diabetes. In non-diabetics, hypertriglyceridaemia and low HDL-cholesterol have been shown to be associated with low plasma adiponectin concentrations. All of these components help to explain why excess abdominal adiposity is considered to be a great threat to cardiovascular and metabolic health.

Adipose tissue as an endocrine organ.