Fibrinolysis in Obesity

Ogston, D.; McAndrew, G. M.

doi:10.1016/s0140-6736(64)91042-6

Cited by 89 publications

(38 citation statements)

References 8 publications

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“…More moderate energy restriction is also associated with marked reductions in FVIIc and PAI-1 (Mehrabian et al, 1990;Folsom et al, 1993;Calles-Escandon et al, 1996). Three studies suggested that these anti-thrombotic effects disappear during subsequent weight maintenance (Ogston & McAndrew, 1964;Svendsen et al, 1996;Baron et al, 1989). These conclusions contrast with our ®ndings.…”

Section: Discussioncontrasting

confidence: 99%

“…These conclusions contrast with our ®ndings. One report was based on observations of only one subject, however (Ogston & McAndrew, 1964). In the study of Svendsen et al, participants were in fact regaining weight ( 2 kg) during follow-up which might explain the ®nding that the initial pro®brinolytic effects disappeared (Svendsen et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…These studies cannot tell whether the bene®cial biochemical effects are primarily explained by the negative energy balance during slimming, or by the reduced body weight. Only few studies included measurements during the maintenance phase following weight loss (Leenen et al, 1993;Ogston & McAndrew, 1964;Baron et al, 1989;Phinney et al, 1991;Wing & Jeffery, 1995;Svendsen et al, 1996). Our knowledge about the late impact of weight reduction on blood lipids and the haemostatic system is therefore limited.…”

Section: Introductionmentioning

confidence: 99%

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Sustained improvement in blood lipids, coagulation, and fibrinolysis after major weight loss in obese subjects

Marckmann¹,

Toubro²,

Astrup³

1998

Eur J Clin Nutr

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Objective: To study whether major weight loss causes sustained improvement in blood lipids and haemostatic pro®le in obese subjects, and to compare the in¯uence of two different slimming and maintenance regimens. Design: Two-stranded randomized intervention study. Setting: University Department. Subjects: Thirty-six out of 43 obese patients recruited from out-patient waiting list completed the study. Interventions: Weight loss was achieved by very low energy formula diet (2 MJad for 8 weeks, n 18), or lowenergy conventional diet (5 MJad for 17 weeks, n 18), both combined with anorectic compound. Participants were re-randomized to consume low fat diet ad libitum (n 16), or energy-restricted diet (n 20) for weight maintenance during 24 weeks. Main outcome measures: Plasma lipids, ®brinogen, factor VII coagulant activity (FVIIc), and plasminogen activator inhibitor type 1 (PAI-1) antigen. Results: Weight loss averaged 13.6 kg (95% CI: 12.3 ± 14.9 kg). After 24 weeks' weight maintenance, plasma total cholesterol was 9% lower, high density lipoprotein cholesterol 5% higher, triglycerides 30% lower, FVIIc 12% lower, ®brinogen 6% lower, and PAI-1 antigen 34% lower than at baseline (all changes highly signi®cant). There were no signi®cant differences between slimming or maintenance regimens. Conclusions: Major weight loss is associated with sustained and marked improvements in blood lipids and hemostatic pro®le, irrespective of the tested slimming and maintenance regimens.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sustained improvement in blood lipids, coagulation, and fibrinolysis after major weight loss in obese subjects

Marckmann¹,

Toubro²,

Astrup³

1998

Eur J Clin Nutr

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“…Association between inflammation and T2DM originated in 1959 when epidemiological studies showed a rise in acute-phase response proteins in serum of type 2 diabetic patients compared with controls (Fearnley et al 1959, Ogston & McAndrew 1964. Later, a specific link between inflammatory and metabolic responses was made with the discovery that compared with lean tissue, obese adipose tissue secretes inflammatory cytokines and that these inflammatory cytokines themselves can inhibit insulin signaling (Hotamisligil et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Alteration of the intestinal barrier and GLP2 secretion in Berberine-treated type 2 diabetic rats

Shan¹,

Yang²,

Yang³

et al. 2013

Journal of Endocrinology

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For centuries, Berberine has been used in the treatment of enteritis in China, and it is also known to have anti-hyperglycemic effects in type 2 diabetic patients. However, as Berberine is insoluble and rarely absorbed in gastrointestinal tract, the mechanism by which it works is unclear. We hypothesized that it may act locally by ameliorating intestinal barrier abnormalities and endotoxemia. A high-fat diet combined with low-dose streptozotocin was used to induce type 2 diabetes in male Sprague Dawley rats. Berberine (100 mg/kg) was administered by lavage to diabetic rats for 2 weeks and saline was given to controls. Hyperinsulinemia and insulin resistance improved in the Berberine group, although there was no significant decrease in blood glucose. Berberine treatment also led to a notable restoration of intestinal villi/mucosa structure and less infiltration of inflammatory cells, along with a decrease in plasma lipopolysaccharide (LPS) level. Tight junction protein zonula occludens 1 (ZO1) was also decreased in diabetic rats but was restored by Berberine treatment. Glutamine-induced glucagon-like peptide 2 (GLP2) secretion from ileal tissue decreased dramatically in the diabetic group but was restored by Berberine treatment. Fasting insulin, insulin resistance index, plasma LPS level, and ZO1 expression were significantly correlated with GLP2 level. In type 2 diabetic rats, Berberine treatment not only augments GLP2 secretion and improves diabetes but is also effective in repairing the damaged intestinal mucosa, restoring intestinal permeability, and improving endotoxemia. Whether these effects are mechanistically related will require further studies, but they certainly support the hypothesis that Berberine acts via modulation of intestinal function.

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“…The underlying molecular mechanism for obesity-related metabolic disorders is still not well understood. The correlation between obesity, diabetes and infl ammation have been observed as early as several decades ago, when increased circulating levels of acute phase proteins, such as fi brinogen, haptoglobin, and α-1 antitripsin, were reported (Fearnley et al 1959;Ogston and McAndrew 1964;Ganrot et al 1967). In more recent studies, elevated serum concentrations of more acute phase proteins were shown, including sialic acid, α-1 acid glycoprotein, C-reactive protein (CRP) and serum amyloid A (Crook et al 1993;Pickup et al 1997).…”

Section: Correlation Between Obesity-related Insulin Resistance and Imentioning

confidence: 99%

Adipose inflammation: cause or consequence of obesity-related insulin resistance

Jiao

Xu²

2008

DMSO

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Obesity constitutes a critical risk factor for the development of many life threatening diseases, particularly insulin resistance and type 2 diabetes. Adipose tissue plays an important role in regulating whole body energy homeostatsis and obesity-related insulin resistance. Infl ammation has been commonly linked to insulin resistance. Recent studies demonstrated that adipose tissue is an important source for producing infl ammatory molecules in the obese state, primarily due to accumulation of macrophages. Animal models defi cient in key infl ammatory molecules or with reduced adipose macrophage infi ltration are protected from development of obesity-related insulin resistance. Repression of adipose infl ammation may be a useful approach to ameliorate obesity-associated metabolic disorders.

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Fibrinolysis in Obesity

Cited by 89 publications

References 8 publications

Sustained improvement in blood lipids, coagulation, and fibrinolysis after major weight loss in obese subjects

Sustained improvement in blood lipids, coagulation, and fibrinolysis after major weight loss in obese subjects

Alteration of the intestinal barrier and GLP2 secretion in Berberine-treated type 2 diabetic rats

Adipose inflammation: cause or consequence of obesity-related insulin resistance

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